Chemokines in Myocardial Infarction

1.

Roth, G. A., Huffman, M. D., Moran, A. E., Feigin, V., Mensah, G. A., Naghavi, M., et al. (2015). Global and regional patterns in cardiovascular mortality from 1990 to 2013. Circulation, 132(17), 1667–1678. https://doi.org/10.1161/CIRCULATIONAHA.114.008720.CrossRefPubMed

2.

Reimer, K. A., Lowe, J. E., Rasmussen, M. M., & Jennings, R. B. (1977). The wavefront phenomenon of ischemic cell death. 1. Myocardial infarct size vs duration of coronary occlusion in dogs. Circulation, 56(5), 786–794.CrossRef

3.

Hjalmarson, A., Elmfeldt, D., Herlitz, J., Holmberg, S., Malek, I., Nyberg, G., et al. (1981). Effect on mortality of metoprolol in acute myocardial infarction. A double-blind randomised trial. Lancet, 2(8251), 823–827. https://doi.org/10.1016/s0140-6736(81)91101-6.CrossRefPubMed

4.

Pfeffer, M. A., Braunwald, E., Moye, L. A., Basta, L., Brown Jr., E. J., Cuddy, T. E., et al. (1992). Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the survival and ventricular enlargement trial. The SAVE Investigators. N Engl J Med, 327(10), 669–677.CrossRef

5.

Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI) (1986). Lancet, 1(8478), 397-402.

6.

Frangogiannis, N. G. (2014). The inflammatory response in myocardial injury, repair, and remodelling. Nature Reviews. Cardiology, 11(5), 255–265. https://doi.org/10.1038/nrcardio.2014.28.CrossRefPubMedPubMedCentral

7.

Cavalera, M., & Frangogiannis, N. G. (2014). Targeting the chemokines in cardiac repair. Current Pharmaceutical Design, 20(12), 1971–1979. https://doi.org/10.2174/13816128113199990449.CrossRefPubMedPubMedCentral

8.

Frangogiannis, N. G. (2007). Chemokines in ischemia and reperfusion. Thrombosis and Haemostasis, 97(5), 738–747.CrossRef

9.

Sokol, C. L., & Luster, A. D. (2015). The chemokine system in innate immunity. Cold Spring Harbor Perspectives in Biology, 7(5). https://doi.org/10.1101/cshperspect.a016303.

10.

Kufareva, I., Salanga, C. L., & Handel, T. M. (2015). Chemokine and chemokine receptor structure and interactions: implications for therapeutic strategies. Immunology and Cell Biology, 93(4), 372–383. https://doi.org/10.1038/icb.2015.15.CrossRefPubMedPubMedCentral

11.

Ahuja, S. K., & Murphy, P. M. (1996). The CXC chemokines growth-regulated oncogene (GRO) alpha, GRObeta, GROgamma, neutrophil-activating peptide-2, and epithelial cell-derived neutrophil-activating peptide-78 are potent agonists for the type B, but not the type A, human interleukin-8 receptor. The Journal of Biological Chemistry, 271(34), 20545–20550. https://doi.org/10.1074/jbc.271.34.20545.CrossRefPubMed

12.

Clark-Lewis, I., Kim, K. S., Rajarathnam, K., Gong, J. H., Dewald, B., Moser, B., et al. (1995). Structure-activity relationships of chemokines. Journal of Leukocyte Biology, 57(5), 703–711. https://doi.org/10.1002/jlb.57.5.703.CrossRefPubMed

13.

Zlotnik, A., Morales, J., & Hedrick, J. A. (1999). Recent advances in chemokines and chemokine receptors. Critical Reviews in Immunology, 19(1), 1–47.PubMed

14.

Zlotnik, A., & Yoshie, O. (2012). The chemokine superfamily revisited. Immunity, 36(5), 705–716. https://doi.org/10.1016/j.immuni.2012.05.008.CrossRefPubMedPubMedCentral

15.

Islam, S. A., Chang, D. S., Colvin, R. A., Byrne, M. H., McCully, M. L., Moser, B., et al. (2011). Mouse CCL8, a CCR8 agonist, promotes atopic dermatitis by recruiting IL-5+ T(H)2 cells. Nature Immunology, 12(2), 167–177. https://doi.org/10.1038/ni.1984.CrossRefPubMed

16.

Jung, S., & Littman, D. R. (1999). Chemokine receptors in lymphoid organ homeostasis. Current Opinion in Immunology, 11(3), 319–325.CrossRef

17.

Murphy, P. M. (1996). Chemokine receptors: structure, function and role in microbial pathogenesis. Cytokine & Growth Factor Reviews, 7(1), 47–64.CrossRef

18.

Weathington, N. M., van Houwelingen, A. H., Noerager, B. D., Jackson, P. L., Kraneveld, A. D., Galin, F. S., et al. (2006). A novel peptide CXCR ligand derived from extracellular matrix degradation during airway inflammation. Nature Medicine, 12(3), 317–323.CrossRef

19.

Bernhagen, J., Krohn, R., Lue, H., Gregory, J. L., Zernecke, A., Koenen, R. R., et al. (2007). MIF is a noncognate ligand of CXC chemokine receptors in inflammatory and atherogenic cell recruitment. Nature Medicine, 13(5), 587–596. https://doi.org/10.1038/nm1567.CrossRefPubMed

20.

Lacy, M., Kontos, C., Brandhofer, M., Hille, K., Groning, S., Sinitski, D., et al. (2018). Identification of an Arg-Leu-Arg tripeptide that contributes to the binding interface between the cytokine MIF and the chemokine receptor CXCR4. Scientific Reports, 8(1), 5171. https://doi.org/10.1038/s41598-018-23554-5.CrossRefPubMedPubMedCentral

21.

Alampour-Rajabi, S., El Bounkari, O., Rot, A., Muller-Newen, G., Bachelerie, F., Gawaz, M., et al. (2015). MIF interacts with CXCR7 to promote receptor internalization, ERK1/2 and ZAP-70 signaling, and lymphocyte chemotaxis. The FASEB Journal, 29(11), 4497–4511. https://doi.org/10.1096/fj.15-273904.CrossRefPubMed

22.

Soppert, J., Kraemer, S., Beckers, C., Averdunk, L., Mollmann, J., Denecke, B., et al. (2018). Soluble CD74 reroutes MIF/CXCR4/AKT-mediated survival of cardiac myofibroblasts to necroptosis. Journal of the American Heart Association, 7(17), e009384. https://doi.org/10.1161/JAHA.118.009384.CrossRefPubMedPubMedCentral

23.

Frangogiannis, N. G. (2012). Regulation of the inflammatory response in cardiac repair. Circulation Research, 110(1), 159–173. https://doi.org/10.1161/CIRCRESAHA.111.243162.CrossRefPubMedPubMedCentral

24.

Chen, B., Huang, S., Su, Y., Wu, Y. J., Hanna, A., Brickshawana, A., et al. (2019). Macrophage Smad3 protects the infarcted heart, stimulating phagocytosis and regulating inflammation. Circulation Research, 125(1), 55–70. https://doi.org/10.1161/CIRCRESAHA.119.315069.CrossRefPubMedPubMedCentral

25.

Shinde, A. V., & Frangogiannis, N. G. (2014). Fibroblasts in myocardial infarction: a role in inflammation and repair. Journal of Molecular and Cellular Cardiology, 70C, 74–82.CrossRef

26.

Kanisicak, O., Khalil, H., Ivey, M. J., Karch, J., Maliken, B. D., Correll, R. N., et al. (2016). Genetic lineage tracing defines myofibroblast origin and function in the injured heart. Nature Communications, 7, 12260. https://doi.org/10.1038/ncomms12260.CrossRefPubMedPubMedCentral

27.

Kong, P., Shinde, A. V., Su, Y., Russo, I., Chen, B., Saxena, A., et al. (2018). Opposing actions of fibroblast and cardiomyocyte Smad3 signaling in the infarcted myocardium. Circulation, 137(7), 707–724. https://doi.org/10.1161/CIRCULATIONAHA.117.029622.CrossRefPubMed

28.

Frangogiannis, N. G., Michael, L. H., & Entman, M. L. (2000). Myofibroblasts in reperfused myocardial infarcts express the embryonic form of smooth muscle myosin heavy chain (SMemb). Cardiovascular Research, 48(1), 89–100.CrossRef

29.

Fu, X., Khalil, H., Kanisicak, O., Boyer, J. G., Vagnozzi, R. J., Maliken, B. D., et al. (2018). Specialized fibroblast differentiated states underlie scar formation in the infarcted mouse heart. The Journal of Clinical Investigation, 128(5), 2127–2143. https://doi.org/10.1172/JCI98215.CrossRefPubMedPubMedCentral

30.

Kakio, T., Matsumori, A., Ono, K., Ito, H., Matsushima, K., & Sasayama, S. (2000). Roles and relationship of macrophages and monocyte chemotactic and activating factor/monocyte chemoattractant protein-1 in the ischemic and reperfused rat heart. Laboratory Investigation, 80(7), 1127–1136.CrossRef

31.

Zouggari, Y., Ait-Oufella, H., Bonnin, P., Simon, T., Sage, A. P., Guerin, C., et al. (2013). B lymphocytes trigger monocyte mobilization and impair heart function after acute myocardial infarction. Nature Medicine, 19(10), 1273–1280.CrossRef

32.

Kumar, A. G., Ballantyne, C. M., Michael, L. H., Kukielka, G. L., Youker, K. A., Lindsey, M. L., et al. (1997). Induction of monocyte chemoattractant protein-1 in the small veins of the ischemic and reperfused canine myocardium. Circulation, 95(3), 693–700.CrossRef

33.

Frangogiannis, N. G., Mendoza, L. H., Lewallen, M., Michael, L. H., Smith, C. W., & Entman, M. L. (2001). Induction and suppression of interferon-inducible protein 10 in reperfused myocardial infarcts may regulate angiogenesis. The FASEB Journal, 15(8), 1428–1430.CrossRef

34.

Mylonas, K. J., Turner, N. A., Bageghni, S. A., Kenyon, C. J., White, C. I., McGregor, K., et al. (2017). 11beta-HSD1 suppresses cardiac fibroblast CXCL2, CXCL5 and neutrophil recruitment to the heart post MI. The Journal of Endocrinology, 233(3), 315–327. https://doi.org/10.1530/JOE-16-0501.CrossRefPubMedPubMedCentral

35.

Turner, N. A., Das, A., O'Regan, D. J., Ball, S. G., & Porter, K. E. (2011). Human cardiac fibroblasts express ICAM-1, E-selectin and CXC chemokines in response to proinflammatory cytokine stimulation. The International Journal of Biochemistry & Cell Biology, 43(10), 1450–1458. https://doi.org/10.1016/j.biocel.2011.06.008.CrossRef

36.

Zymek, P., Nah, D. Y., Bujak, M., Ren, G., Koerting, A., Leucker, T., et al. (2007). Interleukin-10 is not a critical regulator of infarct healing and left ventricular remodeling. Cardiovascular Research, 74(2), 313–322. https://doi.org/10.1016/j.cardiores.2006.11.028.CrossRefPubMed

37.

Muhlstedt, S., Ghadge, S. K., Duchene, J., Qadri, F., Jarve, A., Vilianovich, L., et al. (2016). Cardiomyocyte-derived CXCL12 is not involved in cardiogenesis but plays a crucial role in myocardial infarction. Journal of Molecular Medicine (Berlin, Germany), 94(9), 1005–1014. https://doi.org/10.1007/s00109-016-1432-1.CrossRef

38.

Segret, A., Rucker-Martin, C., Pavoine, C., Flavigny, J., Deroubaix, E., Chatel, M. A., et al. (2007). Structural localization and expression of CXCL12 and CXCR4 in rat heart and isolated cardiac myocytes. The Journal of Histochemistry and Cytochemistry, 55(2), 141–150. https://doi.org/10.1369/jhc.6A7050.2006.CrossRefPubMed

39.

Ban, K., Ikeda, U., Takahashi, M., Kanbe, T., Kasahara, T., & Shimada, K. (1994). Expression of intercellular adhesion molecule-1 on rat cardiac myocytes by monocyte chemoattractant protein-1. Cardiovascular Research, 28(8), 1258–1262.CrossRef

40.

Herzog, C., Lorenz, A., Gillmann, H. J., Chowdhury, A., Larmann, J., Harendza, T., et al. (2014). Thrombomodulin's lectin-like domain reduces myocardial damage by interfering with HMGB1-mediated TLR2 signalling. Cardiovascular Research, 101(3), 400–410. https://doi.org/10.1093/cvr/cvt275.CrossRefPubMed

41.

Andrassy, M., Volz, H. C., Igwe, J. C., Funke, B., Eichberger, S. N., Kaya, Z., et al. (2008). High-mobility group box-1 in ischemia-reperfusion injury of the heart. Circulation, 117(25), 3216–3226.CrossRef

42.

Fiuza, C., Bustin, M., Talwar, S., Tropea, M., Gerstenberger, E., Shelhamer, J. H., et al. (2003). Inflammation-promoting activity of HMGB1 on human microvascular endothelial cells. Blood, 101(7), 2652–2660. https://doi.org/10.1182/blood-2002-05-1300.CrossRefPubMed

43.

Rossini, A., Zacheo, A., Mocini, D., Totta, P., Facchiano, A., Castoldi, R., et al. (2008). HMGB1-stimulated human primary cardiac fibroblasts exert a paracrine action on human and murine cardiac stem cells. Journal of Molecular and Cellular Cardiology, 44(4), 683–693. https://doi.org/10.1016/j.yjmcc.2008.01.009.CrossRefPubMed

44.

Lugrin, J., Parapanov, R., Rosenblatt-Velin, N., Rignault-Clerc, S., Feihl, F., Waeber, B., et al. (2015). Cutting edge: IL-1alpha is a crucial danger signal triggering acute myocardial inflammation during myocardial infarction. Journal of Immunology, 194(2), 499–503. https://doi.org/10.4049/jimmunol.1401948.CrossRef

45.

Chen, C., Feng, Y., Zou, L., Wang, L., Chen, H. H., Cai, J. Y., et al. (2014). Role of extracellular RNA and TLR3-Trif signaling in myocardial ischemia-reperfusion injury. Journal of the American Heart Association, 3(1), e000683. https://doi.org/10.1161/JAHA.113.000683.CrossRefPubMedPubMedCentral

46.

Ghigo, A., Franco, I., Morello, F., & Hirsch, E. (2014). Myocyte signalling in leucocyte recruitment to the heart. Cardiovascular Research, 102(2), 270–280. https://doi.org/10.1093/cvr/cvu030.CrossRefPubMed

47.

Dybdahl, B., Slordahl, S. A., Waage, A., Kierulf, P., Espevik, T., & Sundan, A. (2005). Myocardial ischaemia and the inflammatory response: release of heat shock protein 70 after myocardial infarction. Heart, 91(3), 299–304.CrossRef

48.

Newton, K., & Dixit, V. M. (2012). Signaling in innate immunity and inflammation. Cold Spring Harbor Perspectives in Biology, 4(3). https://doi.org/10.1101/cshperspect.a006049.

49.

Oyama, J., Blais Jr., C., Liu, X., Pu, M., Kobzik, L., Kelly, R. A., et al. (2004). Reduced myocardial ischemia-reperfusion injury in toll-like receptor 4-deficient mice. Circulation, 109(6), 784–789. https://doi.org/10.1161/01.CIR.0000112575.66565.84.CrossRefPubMed

50.

Kaczorowski, D. J., Nakao, A., Mollen, K. P., Vallabhaneni, R., Sugimoto, R., Kohmoto, J., et al. (2007). Toll-like receptor 4 mediates the early inflammatory response after cold ischemia/reperfusion. Transplantation, 84(10), 1279–1287. https://doi.org/10.1097/01.tp.0000287597.87571.17.CrossRefPubMed

51.

Feng, Y., Zhao, H., Xu, X., Buys, E. S., Raher, M. J., Bopassa, J. C., et al. (2008). Innate immune adaptor MyD88 mediates neutrophil recruitment and myocardial injury after ischemia-reperfusion in mice. American Journal of Physiology. Heart and Circulatory Physiology, 295(3), H1311–H1318. https://doi.org/10.1152/ajpheart.00119.2008.CrossRefPubMedPubMedCentral

52.

Ao, L., Zou, N., Cleveland Jr., J. C., Fullerton, D. A., & Meng, X. (2009). Myocardial TLR4 is a determinant of neutrophil infiltration after global myocardial ischemia: mediating KC and MCP-1 expression induced by extracellular HSC70. American Journal of Physiology. Heart and Circulatory Physiology, 297(1), H21–H28. https://doi.org/10.1152/ajpheart.00292.2009.CrossRefPubMedPubMedCentral

53.

Methe, H., Kim, J. O., Kofler, S., Weis, M., Nabauer, M., & Koglin, J. (2005). Expansion of circulating Toll-like receptor 4-positive monocytes in patients with acute coronary syndrome. Circulation, 111(20), 2654–2661. https://doi.org/10.1161/CIRCULATIONAHA.104.498865.CrossRefPubMed

54.

Satoh, M., Shimoda, Y., Maesawa, C., Akatsu, T., Ishikawa, Y., Minami, Y., et al. (2006). Activated toll-like receptor 4 in monocytes is associated with heart failure after acute myocardial infarction. International Journal of Cardiology, 109(2), 226–234. https://doi.org/10.1016/j.ijcard.2005.06.023.CrossRefPubMed

55.

Arslan, F., Smeets, M. B., O'Neill, L. A., Keogh, B., McGuirk, P., Timmers, L., et al. (2010). Myocardial ischemia/reperfusion injury is mediated by leukocytic toll-like receptor-2 and reduced by systemic administration of a novel anti-toll-like receptor-2 antibody. Circulation, 121(1), 80–90.CrossRef

56.

Wang, J. W., Fontes, M. S. C., Wang, X., Chong, S. Y., Kessler, E. L., Zhang, Y. N., et al. (2017). Leukocytic Toll-like receptor 2 deficiency preserves cardiac function and reduces fibrosis in sustained pressure overload. Scientific Reports, 7(1), 9193. https://doi.org/10.1038/s41598-017-09451-3.CrossRefPubMedPubMedCentral

57.

Lu, C., Ren, D., Wang, X., Ha, T., Liu, L., Lee, E. J., et al. (2014). Toll-like receptor 3 plays a role in myocardial infarction and ischemia/reperfusion injury. Biochimica et Biophysica Acta, 1842(1), 22–31.CrossRef

58.

de Kleijn, D. P. V., Chong, S. Y., Wang, X., Yatim, S., Fairhurst, A. M., Vernooij, F., et al. (2019). Toll-like receptor 7 deficiency promotes survival and reduces adverse left ventricular remodelling after myocardial infarction. Cardiovascular Research, 115(12), 1791–1803. https://doi.org/10.1093/cvr/cvz057.CrossRefPubMed

59.

Feng, Y., Chen, H., Cai, J., Zou, L., Yan, D., Xu, G., et al. (2015). Cardiac RNA induces inflammatory responses in cardiomyocytes and immune cells via Toll-like receptor 7 signaling. J Biol Chem, 290(44), 26688-26698, doi:10.1074/jbc. M115.661835.

60.

Frantz, S., Kelly, R. A., & Bourcier, T. (2001). Role of TLR-2 in the activation of nuclear factor kappaB by oxidative stress in cardiac myocytes. The Journal of Biological Chemistry, 276(7), 5197–5203. https://doi.org/10.1074/jbc.M009160200.CrossRefPubMed

61.

Yang, R., Song, Z., Wu, S., Wei, Z., Xu, Y., & Shen, X. (2018). Toll-like receptor 4 contributes to a myofibroblast phenotype in cardiac fibroblasts and is associated with autophagy after myocardial infarction in a mouse model. Atherosclerosis, 279, 23–31. https://doi.org/10.1016/j.atherosclerosis.2018.10.018.CrossRefPubMed

62.

Zhang, W., Lavine, K. J., Epelman, S., Evans, S. A., Weinheimer, C. J., Barger, P. M., et al. (2015). Necrotic myocardial cells release damage-associated molecular patterns that provoke fibroblast activation in vitro and trigger myocardial inflammation and fibrosis in vivo. Journal of the American Heart Association, 4(6), e001993. https://doi.org/10.1161/JAHA.115.001993.CrossRefPubMedPubMedCentral

63.

Li, Y., Si, R., Feng, Y., Chen, H. H., Zou, L., Wang, E., et al. (2011). Myocardial ischemia activates an injurious innate immune signaling via cardiac heat shock protein 60 and Toll-like receptor 4. The Journal of Biological Chemistry, 286(36), 31308–31319.CrossRef

64.

Ritchie, M. E. (1998). Nuclear factor-kappaB is selectively and markedly activated in humans with unstable angina pectoris. Circulation, 98(17), 1707–1713. https://doi.org/10.1161/01.cir.98.17.1707.CrossRefPubMed

65.

Chandrasekar, B., Smith, J. B., & Freeman, G. L. (2001). Ischemia-reperfusion of rat myocardium activates nuclear factor-KappaB and induces neutrophil infiltration via lipopolysaccharide-induced CXC chemokine. Circulation, 103(18), 2296–2302. https://doi.org/10.1161/01.cir.103.18.2296.CrossRefPubMed

66.

Chandrasekar, B., & Freeman, G. L. (1997). Induction of nuclear factor kappaB and activation protein 1 in postischemic myocardium. FEBS Letters, 401(1), 30–34. https://doi.org/10.1016/s0014-5793(96)01426-3.CrossRefPubMed

67.

Onai, Y., Suzuki, J., Kakuta, T., Maejima, Y., Haraguchi, G., Fukasawa, H., et al. (2004). Inhibition of IkappaB phosphorylation in cardiomyocytes attenuates myocardial ischemia/reperfusion injury. Cardiovascular Research, 63(1), 51–59. https://doi.org/10.1016/j.cardiores.2004.03.002.CrossRefPubMed

68.

Li, H. L., Zhuo, M. L., Wang, D., Wang, A. B., Cai, H., Sun, L. H., et al. (2007). Targeted cardiac overexpression of A20 improves left ventricular performance and reduces compensatory hypertrophy after myocardial infarction. Circulation, 115(14), 1885–1894. https://doi.org/10.1161/CIRCULATIONAHA.106.656835.CrossRefPubMed

69.

Timmers, L., van Keulen, J. K., Hoefer, I. E., Meijs, M. F., van Middelaar, B., den Ouden, K., et al. (2009). Targeted deletion of nuclear factor kappaB p50 enhances cardiac remodeling and dysfunction following myocardial infarction. Circulation Research, 104(5), 699–706. https://doi.org/10.1161/CIRCRESAHA.108.189746.CrossRefPubMed

70.

Frantz, S., Tillmanns, J., Kuhlencordt, P. J., Schmidt, I., Adamek, A., Dienesch, C., et al. (2007). Tissue-specific effects of the nuclear factor kappaB subunit p50 on myocardial ischemia-reperfusion injury. The American Journal of Pathology, 171(2), 507–512. https://doi.org/10.2353/ajpath.2007.061042.CrossRefPubMedPubMedCentral

71.

Pinckard, R. N., Olson, M. S., Giclas, P. C., Terry, R., Boyer, J. T., & O'Rourke, R. A. (1975). Consumption of classical complement components by heart subcellular membranes in vitro and in patients after acute myocardial infarction. The Journal of Clinical Investigation, 56(3), 740–750. https://doi.org/10.1172/JCI108145.CrossRefPubMedPubMedCentral

72.

Hill, J. H., & Ward, P. A. (1971). The phlogistic role of C3 leukotactic fragments in myocardial infarcts of rats. The Journal of Experimental Medicine, 133(4), 885–900. https://doi.org/10.1084/jem.133.4.885.CrossRefPubMedPubMedCentral

73.

Czermak, B. J., Sarma, V., Bless, N. M., Schmal, H., Friedl, H. P., & Ward, P. A. (1999). In vitro and in vivo dependency of chemokine generation on C5a and TNF-alpha. Journal of Immunology, 162(4), 2321–2325.

74.

Kilgore, K. S., Park, J. L., Tanhehco, E. J., Booth, E. A., Marks, R. M., & Lucchesi, B. R. (1998). Attenuation of interleukin-8 expression in C6-deficient rabbits after myocardial ischemia/reperfusion. Journal of Molecular and Cellular Cardiology, 30(1), 75–85. https://doi.org/10.1006/jmcc.1997.0573.CrossRefPubMed

75.

Maekawa, N., Wada, H., Kanda, T., Niwa, T., Yamada, Y., Saito, K., et al. (2002). Improved myocardial ischemia/reperfusion injury in mice lacking tumor necrosis factor-alpha. Journal of the American College of Cardiology, 39(7), 1229–1235. https://doi.org/10.1016/s0735-1097(02)01738-2.CrossRefPubMed

76.

Bujak, M., Dobaczewski, M., Chatila, K., Mendoza, L. H., Li, N., Reddy, A., et al. (2008). Interleukin-1 receptor type I signaling critically regulates infarct healing and cardiac remodeling. The American Journal of Pathology, 173(1), 57–67. https://doi.org/10.2353/ajpath.2008.070974.CrossRefPubMedPubMedCentral

77.

Saxena, A., Chen, W., Su, Y., Rai, V., Uche, O. U., Li, N., et al. (2013). IL-1 induces proinflammatory leukocyte infiltration and regulates fibroblast phenotype in the infarcted myocardium. Journal of Immunology, 191(9), 4838–4848. https://doi.org/10.4049/jimmunol.1300725.CrossRef

78.

Frangogiannis, N. G., Lindsey, M. L., Michael, L. H., Youker, K. A., Bressler, R. B., Mendoza, L. H., et al. (1998). Resident cardiac mast cells degranulate and release preformed TNF-alpha, initiating the cytokine cascade in experimental canine myocardial ischemia/reperfusion. Circulation, 98(7), 699–710. https://doi.org/10.1161/01.cir.98.7.699.CrossRefPubMed

79.

Somasundaram, P., Ren, G., Nagar, H., Kraemer, D., Mendoza, L., Michael, L. H., et al. (2005). Mast cell tryptase may modulate endothelial cell phenotype in healing myocardial infarcts. The Journal of Pathology, 205(1), 102–111. https://doi.org/10.1002/path.1690.CrossRefPubMedPubMedCentral

80.

Oynebraten, I., Bakke, O., Brandtzaeg, P., Johansen, F. E., & Haraldsen, G. (2004). Rapid chemokine secretion from endothelial cells originates from 2 distinct compartments. Blood, 104(2), 314–320. https://doi.org/10.1182/blood-2003-08-2891.CrossRefPubMed

81.

Detmers, P. A., Lo, S. K., Olsen-Egbert, E., Walz, A., Baggiolini, M., & Cohn, Z. A. (1990). Neutrophil-activating protein 1/interleukin 8 stimulates the binding activity of the leukocyte adhesion receptor CD11b/CD18 on human neutrophils. The Journal of Experimental Medicine, 171(4), 1155–1162. https://doi.org/10.1084/jem.171.4.1155.CrossRefPubMed

82.

Herter, J., & Zarbock, A. (2013). Integrin regulation during leukocyte recruitment. Journal of Immunology, 190(9), 4451–4457. https://doi.org/10.4049/jimmunol.1203179.CrossRef

83.

Knall, C., Worthen, G. S., & Johnson, G. L. (1997). Interleukin 8-stimulated phosphatidylinositol-3-kinase activity regulates the migration of human neutrophils independent of extracellular signal-regulated kinase and p38 mitogen-activated protein kinases. Proceedings of the National Academy of Sciences of the United States of America, 94(7), 3052–3057. https://doi.org/10.1073/pnas.94.7.3052.CrossRefPubMedPubMedCentral

84.

Legler, D. F., & Thelen, M. (2018). New insights in chemokine signaling. F1000Res, 7, 95, doi:https://doi.org/10.12688/f1000research.13130.1.

85.

Sotsios, Y., & Ward, S. G. (2000). Phosphoinositide 3-kinase: a key biochemical signal for cell migration in response to chemokines. Immunological Reviews, 177, 217–235.CrossRef

86.

Bujak, M., Dobaczewski, M., Gonzalez-Quesada, C., Xia, Y., Leucker, T., Zymek, P., et al. (2009). Induction of the CXC chemokine interferon-gamma-inducible protein 10 regulates the reparative response following myocardial infarction. Circulation Research, 105(10), 973–983. https://doi.org/10.1161/CIRCRESAHA.109.199471.CrossRefPubMedPubMedCentral

87.

Tarzami, S. T., Miao, W., Mani, K., Lopez, L., Factor, S. M., Berman, J. W., et al. (2003). Opposing effects mediated by the chemokine receptor CXCR2 on myocardial ischemia-reperfusion injury: recruitment of potentially damaging neutrophils and direct myocardial protection. Circulation, 108(19), 2387–2392. https://doi.org/10.1161/01.CIR.0000093192.72099.9A.CrossRefPubMed

88.

Jarrah, A. A., Schwarskopf, M., Wang, E. R., LaRocca, T., Dhume, A., Zhang, S., et al. (2018). SDF-1 induces TNF-mediated apoptosis in cardiac myocytes. Apoptosis, 23(1), 79–91. https://doi.org/10.1007/s10495-017-1438-3.CrossRefPubMedPubMedCentral

89.

Strieter, R. M., Polverini, P. J., Kunkel, S. L., Arenberg, D. A., Burdick, M. D., Kasper, J., et al. (1995). The functional role of the ELR motif in CXC chemokine-mediated angiogenesis. The Journal of Biological Chemistry, 270(45), 27348–27357.CrossRef

90.

Kukielka, G. L., Smith, C. W., LaRosa, G. J., Manning, A. M., Mendoza, L. H., Daly, T. J., et al. (1995). Interleukin-8 gene induction in the myocardium after ischemia and reperfusion in vivo. The Journal of Clinical Investigation, 95(1), 89–103. https://doi.org/10.1172/JCI117680.CrossRefPubMedPubMedCentral

91.

Ivey, C. L., Williams, F. M., Collins, P. D., Jose, P. J., & Williams, T. J. (1995). Neutrophil chemoattractants generated in two phases during reperfusion of ischemic myocardium in the rabbit. Evidence for a role for C5a and interleukin-8. The Journal of Clinical Investigation, 95(6), 2720–2728. https://doi.org/10.1172/JCI117974.CrossRefPubMedPubMedCentral

92.

Zeilhofer, H. U., & Schorr, W. (2000). Role of interleukin-8 in neutrophil signaling. Current Opinion in Hematology, 7(3), 178–182.CrossRef

93.

Boyle Jr., E. M., Kovacich, J. C., Hebert, C. A., Canty Jr., T. G., Chi, E., Morgan, E. N., et al. (1998). Inhibition of interleukin-8 blocks myocardial ischemia-reperfusion injury. The Journal of Thoracic and Cardiovascular Surgery, 116(1), 114–121. https://doi.org/10.1016/S0022-5223(98)70249-1.CrossRefPubMed

94.

Oral, H., Kanzler, I., Tuchscheerer, N., Curaj, A., Simsekyilmaz, S., Sonmez, T. T., et al. (2013). CXC chemokine KC fails to induce neutrophil infiltration and neoangiogenesis in a mouse model of myocardial infarction. Journal of Molecular and Cellular Cardiology, 60, 1–7. https://doi.org/10.1016/j.yjmcc.2013.04.006.CrossRefPubMed

95.

Xie, Q., Sun, Z., Chen, M., Zhong, Q., Yang, T., & Yi, J. (2015). IL-8 up-regulates proliferative angiogenesis in ischemic myocardium in rabbits through phosphorylation of Akt/GSK-3beta(ser9) dependent pathways. International Journal of Clinical and Experimental Medicine, 8(8), 12498–12508.PubMedPubMedCentral

96.

Shetelig, C., Limalanathan, S., Hoffmann, P., Seljeflot, I., Gran, J. M., Eritsland, J., et al. (2018). Association of IL-8 with infarct size and clinical outcomes in patients With STEMI. Journal of the American College of Cardiology, 72(2), 187–198. https://doi.org/10.1016/j.jacc.2018.04.053.CrossRefPubMed

97.

Moser, B., & Loetscher, P. (2001). Lymphocyte traffic control by chemokines. Nature Immunology, 2(2), 123–128. https://doi.org/10.1038/84219.CrossRefPubMed

98.

Fiorina, P., Ansari, M. J., Jurewicz, M., Barry, M., Ricchiuti, V., Smith, R. N., et al. (2006). Role of CXC chemokine receptor 3 pathway in renal ischemic injury. J Am Soc Nephrol, 17(3), 716–723. https://doi.org/10.1681/ASN.2005090954.CrossRefPubMed

99.

Khan, I. A., MacLean, J. A., Lee, F. S., Casciotti, L., DeHaan, E., Schwartzman, J. D., et al. (2000). IP-10 is critical for effector T cell trafficking and host survival in Toxoplasma gondii infection. Immunity, 12(5), 483–494. https://doi.org/10.1016/s1074-7613(00)80200-9.CrossRefPubMed

100.

Shiraha, H., Glading, A., Gupta, K., & Wells, A. (1999). IP-10 inhibits epidermal growth factor-induced motility by decreasing epidermal growth factor receptor-mediated calpain activity. The Journal of Cell Biology, 146(1), 243–254. https://doi.org/10.1083/jcb.146.1.243.CrossRefPubMedPubMedCentral

101.

Strieter, R. M., Polverini, P. J., Arenberg, D. A., Walz, A., Opdenakker, G., Van Damme, J., et al. (1995). Role of C-X-C chemokines as regulators of angiogenesis in lung cancer. Journal of Leukocyte Biology, 57(5), 752–762. https://doi.org/10.1002/jlb.57.5.752.CrossRefPubMed

102.

Strieter, R. M., Polverini, P. J., Kunkel, S. L., Arenberg, D. A., Burdick, M. D., Kasper, J., et al. (1995). The functional role of the ELR motif in CXC chemokine-mediated angiogenesis. The Journal of Biological Chemistry, 270(45), 27348–27357. https://doi.org/10.1074/jbc.270.45.27348.CrossRefPubMed

103.

Dewald, O., Ren, G., Duerr, G. D., Zoerlein, M., Klemm, C., Gersch, C., et al. (2004). Of mice and dogs: species-specific differences in the inflammatory response following myocardial infarction. The American Journal of Pathology, 164(2), 665–677. https://doi.org/10.1016/S0002-9440(10)63154-9.CrossRefPubMedPubMedCentral

104.

Loetscher, M., Gerber, B., Loetscher, P., Jones, S. A., Piali, L., Clark-Lewis, I., et al. (1996). Chemokine receptor specific for IP10 and mig: structure, function, and expression in activated T-lymphocytes. The Journal of Experimental Medicine, 184(3), 963–969. https://doi.org/10.1084/jem.184.3.963.CrossRefPubMed

105.

Saxena, A., Bujak, M., Frunza, O., Dobaczewski, M., Gonzalez-Quesada, C., Lu, B., et al. (2014). CXCR3-independent actions of the CXC chemokine CXCL10 in the infarcted myocardium and in isolated cardiac fibroblasts are mediated through proteoglycans. Cardiovascular Research, 103(2), 217–227. https://doi.org/10.1093/cvr/cvu138.CrossRefPubMedPubMedCentral

106.

Nagasawa, T., Hirota, S., Tachibana, K., Takakura, N., Nishikawa, S., Kitamura, Y., et al. (1996). Defects of B cell lymphopoiesis and bone-marrow myelopoiesis in mice lacking the CXC chemokine PBSF/SDF-1. Nature, 382(6592), 635–638. https://doi.org/10.1038/382635a0.CrossRefPubMed

107.

Salvucci, O., Yao, L., Villalba, S., Sajewicz, A., Pittaluga, S., & Tosato, G. (2002). Regulation of endothelial cell branching morphogenesis by endogenous chemokine stromal-derived factor-1. Blood, 99(8), 2703–2711. https://doi.org/10.1182/blood.v99.8.2703.CrossRefPubMed

108.

Salcedo, R., Wasserman, K., Young, H. A., Grimm, M. C., Howard, O. M., Anver, M. R., et al. (1999). Vascular endothelial growth factor and basic fibroblast growth factor induce expression of CXCR4 on human endothelial cells: In vivo neovascularization induced by stromal-derived factor-1alpha. The American Journal of Pathology, 154(4), 1125–1135. https://doi.org/10.1016/s0002-9440(10)65365-5.CrossRefPubMedPubMedCentral

109.

Pillarisetti, K., & Gupta, S. K. (2001). Cloning and relative expression analysis of rat stromal cell derived factor-1 (SDF-1)1: SDF-1 alpha mRNA is selectively induced in rat model of myocardial infarction. Inflammation, 25(5), 293–300. https://doi.org/10.1023/a:1012808525370.CrossRefPubMed

110.

Askari, A. T., Unzek, S., Popovic, Z. B., Goldman, C. K., Forudi, F., Kiedrowski, M., et al. (2003). Effect of stromal-cell-derived factor 1 on stem-cell homing and tissue regeneration in ischaemic cardiomyopathy. Lancet, 362(9385), 697–703. https://doi.org/10.1016/S0140-6736(03)14232-8.CrossRefPubMed

111.

Frangogiannis, N. G. (2011). The stromal cell-derived factor-1/CXCR4 axis in cardiac injury and repair. Journal of the American College of Cardiology, 58(23), 2424–2426. https://doi.org/10.1016/j.jacc.2011.08.031.CrossRefPubMed

112.

Uematsu, M., Yoshizaki, T., Shimizu, T., Obata, J. E., Nakamura, T., Fujioka, D., et al. (2015). Sustained myocardial production of stromal cell-derived factor-1alpha was associated with left ventricular adverse remodeling in patients with myocardial infarction. American Journal of Physiology. Heart and Circulatory Physiology, 309(10), H1764–H1771. https://doi.org/10.1152/ajpheart.00493.2015.CrossRefPubMed

113.

Ceradini, D. J., Kulkarni, A. R., Callaghan, M. J., Tepper, O. M., Bastidas, N., Kleinman, M. E., et al. (2004). Progenitor cell trafficking is regulated by hypoxic gradients through HIF-1 induction of SDF-1. Nature Medicine, 10(8), 858–864. https://doi.org/10.1038/nm1075.CrossRefPubMed

114.

Abbott, J. D., Huang, Y., Liu, D., Hickey, R., Krause, D. S., & Giordano, F. J. (2004). Stromal cell-derived factor-1alpha plays a critical role in stem cell recruitment to the heart after myocardial infarction but is not sufficient to induce homing in the absence of injury. Circulation, 110(21), 3300–3305. https://doi.org/10.1161/01.CIR.0000147780.30124.CF.CrossRefPubMed

115.

Ma, J., Ge, J., Zhang, S., Sun, A., Shen, J., Chen, L., et al. (2005). Time course of myocardial stromal cell-derived factor 1 expression and beneficial effects of intravenously administered bone marrow stem cells in rats with experimental myocardial infarction. Basic Research in Cardiology, 100(3), 217–223. https://doi.org/10.1007/s00395-005-0521-z.CrossRefPubMed

116.

Saxena, A., Fish, J. E., White, M. D., Yu, S., Smyth, J. W., Shaw, R. M., et al. (2008). Stromal cell-derived factor-1alpha is cardioprotective after myocardial infarction. Circulation, 117(17), 2224–2231. https://doi.org/10.1161/CIRCULATIONAHA.107.694992.CrossRefPubMedPubMedCentral

117.

Zhang, M., Mal, N., Kiedrowski, M., Chacko, M., Askari, A. T., Popovic, Z. B., et al. (2007). SDF-1 expression by mesenchymal stem cells results in trophic support of cardiac myocytes after myocardial infarction. The FASEB Journal, 21(12), 3197–3207. https://doi.org/10.1096/fj.06-6558com.CrossRefPubMed

118.

Sasaki, T., Fukazawa, R., Ogawa, S., Kanno, S., Nitta, T., Ochi, M., et al. (2007). Stromal cell-derived factor-1alpha improves infarcted heart function through angiogenesis in mice. Pediatrics International, 49(6), 966–971. https://doi.org/10.1111/j.1442-200X.2007.02491.x.CrossRefPubMed

119.

MacArthur Jr., J. W., Purcell, B. P., Shudo, Y., Cohen, J. E., Fairman, A., Trubelja, A., et al. (2013). Sustained release of engineered stromal cell-derived factor 1-alpha from injectable hydrogels effectively recruits endothelial progenitor cells and preserves ventricular function after myocardial infarction. Circulation, 128(11 Suppl 1), S79–S86. https://doi.org/10.1161/CIRCULATIONAHA.112.000343.CrossRefPubMedPubMedCentral

120.

Macarthur Jr., J. W., Cohen, J. E., McGarvey, J. R., Shudo, Y., Patel, J. B., Trubelja, A., et al. (2014). Preclinical evaluation of the engineered stem cell chemokine stromal cell-derived factor 1alpha analog in a translational ovine myocardial infarction model. Circulation Research, 114(4), 650–659. https://doi.org/10.1161/CIRCRESAHA.114.302884.CrossRefPubMed

121.

Elmadbouh, I., Haider, H., Jiang, S., Idris, N. M., Lu, G., & Ashraf, M. (2007). Ex vivo delivered stromal cell-derived factor-1alpha promotes stem cell homing and induces angiomyogenesis in the infarcted myocardium. Journal of Molecular and Cellular Cardiology, 42(4), 792–803. https://doi.org/10.1016/j.yjmcc.2007.02.001.CrossRefPubMedPubMedCentral

122.

Mayorga, M. E., Kiedrowski, M., McCallinhart, P., Forudi, F., Ockunzzi, J., Weber, K., et al. (2018). Role of SDF-1:CXCR4 in impaired post-myocardial infarction cardiac repair in diabetes. Stem Cells Translational Medicine, 7(1), 115–124. https://doi.org/10.1002/sctm.17-0172.CrossRefPubMed

123.

Cheng, M., Huang, K., Zhou, J., Yan, D., Tang, Y. L., Zhao, T. C., et al. (2015). A critical role of Src family kinase in SDF-1/CXCR4-mediated bone-marrow progenitor cell recruitment to the ischemic heart. Journal of Molecular and Cellular Cardiology, 81, 49–53. https://doi.org/10.1016/j.yjmcc.2015.01.024.CrossRefPubMedPubMedCentral

124.

Wang, M., Hu, R., Yang, Y., Xiang, L., & Mu, Y. (2019). In vivo ultrasound molecular imaging of SDF-1 expression in a swine model of acute myocardial infarction. Frontiers in Pharmacology, 10, 899. https://doi.org/10.3389/fphar.2019.00899.CrossRefPubMedPubMedCentral

125.

Huang, F. Y., Xia, T. L., Li, J. L., Li, C. M., Zhao, Z. G., Lei, W. H., et al. (2019). The bifunctional SDF-1-AnxA5 fusion protein protects cardiac function after myocardial infarction. Journal of Cellular and Molecular Medicine, 23(11), 7673–7684. https://doi.org/10.1111/jcmm.14640.CrossRefPubMedPubMedCentral

126.

Goldstone, A. B., Burnett, C. E., Cohen, J. E., Paulsen, M. J., Eskandari, A., Edwards, B. E., et al. (2018). SDF 1-alpha attenuates myocardial injury without altering the direct contribution of circulating cells. Journal of Cardiovascular Translational Research, 11(4), 274–284. https://doi.org/10.1007/s12265-017-9772-y.CrossRefPubMedPubMedCentral

127.

Liu, Y., Gao, S., Wang, Z., Yang, Y., Huo, H., & Tian, X. (2016). Effect of stromal cell-derived factor-1 on myocardial apoptosis and cardiac function recovery in rats with acute myocardial infarction. Experimental and Therapeutic Medicine, 12(5), 3282–3286. https://doi.org/10.3892/etm.2016.3770.CrossRefPubMedPubMedCentral

128.

Hu, X., Dai, S., Wu, W. J., Tan, W., Zhu, X., Mu, J., et al. (2007). Stromal cell derived factor-1 alpha confers protection against myocardial ischemia/reperfusion injury: role of the cardiac stromal cell derived factor-1 alpha CXCR4 axis. Circulation, 116(6), 654–663. https://doi.org/10.1161/CIRCULATIONAHA.106.672451.CrossRefPubMedPubMedCentral

129.

Chen, J., Chemaly, E., Liang, L., Kho, C., Lee, A., Park, J., et al. (2010). Effects of CXCR4 gene transfer on cardiac function after ischemia-reperfusion injury. The American Journal of Pathology, 176(4), 1705–1715. https://doi.org/10.2353/ajpath.2010.090451.CrossRefPubMedPubMedCentral

130.

Dai, S., Yuan, F., Mu, J., Li, C., Chen, N., Guo, S., et al. (2010). Chronic AMD3100 antagonism of SDF-1alpha-CXCR4 exacerbates cardiac dysfunction and remodeling after myocardial infarction. Journal of Molecular and Cellular Cardiology, 49(4), 587–597. https://doi.org/10.1016/j.yjmcc.2010.07.010.CrossRefPubMedPubMedCentral

131.

Proulx, C., El-Helou, V., Gosselin, H., Clement, R., Gillis, M. A., Villeneuve, L., et al. (2007). Antagonism of stromal cell-derived factor-1alpha reduces infarct size and improves ventricular function after myocardial infarction. Pflügers Archiv, 455(2), 241–250. https://doi.org/10.1007/s00424-007-0284-5.CrossRefPubMed

132.

Jujo, K., Hamada, H., Iwakura, A., Thorne, T., Sekiguchi, H., Clarke, T., et al. (2010). CXCR4 blockade augments bone marrow progenitor cell recruitment to the neovasculature and reduces mortality after myocardial infarction. Proceedings of the National Academy of Sciences of the United States of America, 107(24), 11008–11013. https://doi.org/10.1073/pnas.0914248107.CrossRefPubMedPubMedCentral

133.

Hao, H., Hu, S., Chen, H., Bu, D., Zhu, L., Xu, C., et al. (2017). Loss of endothelial CXCR7 impairs vascular homeostasis and cardiac remodeling after myocardial infarction: implications for cardiovascular drug discovery. Circulation, 135(13), 1253–1264. https://doi.org/10.1161/CIRCULATIONAHA.116.023027.CrossRefPubMed

134.

Das, S., Goldstone, A. B., Wang, H., Farry, J., D'Amato, G., Paulsen, M. J., et al. (2019). A unique collateral artery development program promotes neonatal heart regeneration. Cell, 176(5), 1128-1142 e1118, doi:https://doi.org/10.1016/j.cell.2018.12.023.

135.

Dewald, O., Zymek, P., Winkelmann, K., Koerting, A., Ren, G., Abou-Khamis, T., et al. (2005). CCL2/Monocyte chemoattractant protein-1 regulates inflammatory responses critical to healing myocardial infarcts. Circulation Research, 96(8), 881–889. https://doi.org/10.1161/01.RES.0000163017.13772.3a.CrossRefPubMed

136.

Ono, K., Matsumori, A., Furukawa, Y., Igata, H., Shioi, T., Matsushima, K., et al. (1999). Prevention of myocardial reperfusion injury in rats by an antibody against monocyte chemotactic and activating factor/monocyte chemoattractant protein-1. Laboratory Investigation, 79(2), 195–203.PubMed

137.

Tarzami, S. T., Cheng, R., Miao, W., Kitsis, R. N., & Berman, J. W. (2002). Chemokine expression in myocardial ischemia: MIP-2 dependent MCP-1 expression protects cardiomyocytes from cell death. Journal of Molecular and Cellular Cardiology, 34(2), 209–221. https://doi.org/10.1006/jmcc.2001.1503.CrossRefPubMed

138.

Pinto, A. R., Ilinykh, A., Ivey, M. J., Kuwabara, J. T., D’Antoni, M. L., Debuque, R., et al. (2016). Revisiting cardiac cellular composition. Circulation Research, 118(3), 400–409. https://doi.org/10.1161/CIRCRESAHA.115.307778.CrossRefPubMed

139.

Epelman, S., Lavine, K. J., Beaudin, A. E., Sojka, D. K., Carrero, J. A., Calderon, B., et al. (2014). Embryonic and adult-derived resident cardiac macrophages are maintained through distinct mechanisms at steady state and during inflammation. Immunity, 40(1), 91–104. https://doi.org/10.1016/j.immuni.2013.11.019.CrossRefPubMedPubMedCentral

140.

Epelman, S., Lavine, K. J., & Randolph, G. J. (2014). Origin and functions of tissue macrophages. Immunity, 41(1), 21–35. https://doi.org/10.1016/j.immuni.2014.06.013.CrossRefPubMedPubMedCentral

141.

Lavine, K. J., Epelman, S., Uchida, K., Weber, K. J., Nichols, C. G., Schilling, J. D., et al. (2014). Distinct macrophage lineages contribute to disparate patterns of cardiac recovery and remodeling in the neonatal and adult heart. Proceedings of the National Academy of Sciences of the United States of America, 111(45), 16029–16034. https://doi.org/10.1073/pnas.1406508111.CrossRefPubMedPubMedCentral

142.

Leid, J., Carrelha, J., Boukarabila, H., Epelman, S., Jacobsen, S. E., & Lavine, K. J. (2016). Primitive embryonic macrophages are required for coronary development and maturation. Circulation Research, 118(10), 1498–1511. https://doi.org/10.1161/CIRCRESAHA.115.308270.CrossRefPubMedPubMedCentral

143.

Bajpai, G., Bredemeyer, A., Li, W., Zaitsev, K., Koenig, A. L., Lokshina, I., et al. (2019). Tissue resident CCR2- and CCR2+ cardiac macrophages differentially orchestrate monocyte recruitment and fate specification following myocardial injury. Circulation Research, 124(2), 263–278. https://doi.org/10.1161/CIRCRESAHA.118.314028.CrossRefPubMedPubMedCentral

144.

Heidt, T., Courties, G., Dutta, P., Sager, H. B., Sebas, M., Iwamoto, Y., et al. (2014). Differential contribution of monocytes to heart macrophages in steady-state and after myocardial infarction. Circulation Research, 115(2), 284–295. https://doi.org/10.1161/CIRCRESAHA.115.303567.CrossRefPubMedPubMedCentral

145.

Frangogiannis, N. G., Mendoza, L. H., Ren, G., Akrivakis, S., Jackson, P. L., Michael, L. H., et al. (2003). MCSF expression is induced in healing myocardial infarcts and may regulate monocyte and endothelial cell phenotype. American Journal of Physiology. Heart and Circulatory Physiology, 285(2), H483–H492.CrossRef

146.

Sager, H. B., Hulsmans, M., Lavine, K. J., Moreira, M. B., Heidt, T., Courties, G., et al. (2016). Proliferation and recruitment contribute to myocardial macrophage expansion in chronic heart failure. Circulation Research, 119(7), 853–864. https://doi.org/10.1161/CIRCRESAHA.116.309001.CrossRefPubMedPubMedCentral

147.

Liehn, E. A., Piccinini, A. M., Koenen, R. R., Soehnlein, O., Adage, T., Fatu, R., et al. (2010). A new monocyte chemotactic protein-1/chemokine CC motif ligand-2 competitor limiting neointima formation and myocardial ischemia/reperfusion injury in mice. Journal of the American College of Cardiology, 56(22), 1847–1857. https://doi.org/10.1016/j.jacc.2010.04.066.CrossRefPubMed

148.

Al-Amran, F. G., Manson, M. Z., Hanley, T. K., & Hainz, D. L. (2014). Blockade of the monocyte chemoattractant protein-1 receptor pathway ameliorates myocardial injury in animal models of ischemia and reperfusion. Pharmacology, 93(5-6), 296–302. https://doi.org/10.1159/000363657.CrossRefPubMed

149.

Grisanti, L. A., Traynham, C. J., Repas, A. A., Gao, E., Koch, W. J., & Tilley, D. G. (2016). beta2-Adrenergic receptor-dependent chemokine receptor 2 expression regulates leukocyte recruitment to the heart following acute injury. Proceedings of the National Academy of Sciences of the United States of America, 113(52), 15126–15131. https://doi.org/10.1073/pnas.1611023114.CrossRefPubMedPubMedCentral

150.

Wang, J., Seo, M. J., Deci, M. B., Weil, B. R., Canty, J. M., & Nguyen, J. (2018). Effect of CCR2 inhibitor-loaded lipid micelles on inflammatory cell migration and cardiac function after myocardial infarction. International Journal of Nanomedicine, 13, 6441–6451. https://doi.org/10.2147/IJN.S178650.CrossRefPubMedPubMedCentral

151.

Leuschner, F., Dutta, P., Gorbatov, R., Novobrantseva, T. I., Donahoe, J. S., Courties, G., et al. (2011). Therapeutic siRNA silencing in inflammatory monocytes in mice. Nature Biotechnology, 29(11), 1005–1010. https://doi.org/10.1038/nbt.1989.CrossRefPubMedPubMedCentral

152.

Lu, W., Xie, Z., Tang, Y., Bai, L., Yao, Y., Fu, C., et al. (2015). Photoluminescent mesoporous silicon nanoparticles with siCCR2 improve the effects of mesenchymal stromal cell transplantation after acute myocardial infarction. Theranostics, 5(10), 1068–1082. https://doi.org/10.7150/thno.11517.CrossRefPubMedPubMedCentral

153.

Kaikita, K., Hayasaki, T., Okuma, T., Kuziel, W. A., Ogawa, H., & Takeya, M. (2004). Targeted deletion of CC chemokine receptor 2 attenuates left ventricular remodeling after experimental myocardial infarction. The American Journal of Pathology, 165(2), 439–447. https://doi.org/10.1016/S0002-9440(10)63309-3.CrossRefPubMedPubMedCentral

154.

Nahrendorf, M., Swirski, F. K., Aikawa, E., Stangenberg, L., Wurdinger, T., Figueiredo, J. L., et al. (2007). The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions. The Journal of Experimental Medicine, 204(12), 3037–3047. https://doi.org/10.1084/jem.20070885.CrossRefPubMedPubMedCentral

155.

Gavrilin, M. A., Deucher, M. F., Boeckman, F., & Kolattukudy, P. E. (2000). Monocyte chemotactic protein 1 upregulates IL-1beta expression in human monocytes. Biochemical and Biophysical Research Communications, 277(1), 37–42. https://doi.org/10.1006/bbrc.2000.3619.CrossRefPubMed

156.

Jiang, Y., Beller, D. I., Frendl, G., & Graves, D. T. (1992). Monocyte chemoattractant protein-1 regulates adhesion molecule expression and cytokine production in human monocytes. Journal of Immunology, 148(8), 2423–2428.

157.

Sierra-Filardi, E., Nieto, C., Dominguez-Soto, A., Barroso, R., Sanchez-Mateos, P., Puig-Kroger, A., et al. (2014). CCL2 shapes macrophage polarization by GM-CSF and M-CSF: identification of CCL2/CCR2-dependent gene expression profile. Journal of Immunology, 192(8), 3858–3867. https://doi.org/10.4049/jimmunol.1302821.CrossRef

158.

Frangogiannis, N. G., Dewald, O., Xia, Y., Ren, G., Haudek, S., Leucker, T., et al. (2007). Critical role of monocyte chemoattractant protein-1/CC chemokine ligand 2 in the pathogenesis of ischemic cardiomyopathy. Circulation, 115(5), 584–592.CrossRef

159.

Schenk, S., Mal, N., Finan, A., Zhang, M., Kiedrowski, M., Popovic, Z., et al. (2007). Monocyte chemotactic protein-3 is a myocardial mesenchymal stem cell homing factor. Stem Cells, 25(1), 245–251. https://doi.org/10.1634/stemcells.2006-0293.CrossRefPubMed

160.

Montecucco, F., Braunersreuther, V., Lenglet, S., Delattre, B. M., Pelli, G., Buatois, V., et al. (2012). CC chemokine CCL5 plays a central role impacting infarct size and post-infarction heart failure in mice. European Heart Journal, 33(15), 1964–1974. https://doi.org/10.1093/eurheartj/ehr127.CrossRefPubMed

161.

Huang, Y., Wang, D., Wang, X., Zhang, Y., Liu, T., Chen, Y., et al. (2016). Abrogation of CC chemokine receptor 9 ameliorates ventricular remodeling in mice after myocardial infarction. Scientific Reports, 6, 32660. https://doi.org/10.1038/srep32660.CrossRefPubMedPubMedCentral

162.

Jiang, Y., Bai, J., Tang, L., Zhang, P., & Pu, J. (2015). Anti-CCL21 antibody attenuates infarct size and improves cardiac remodeling after myocardial infarction. Cellular Physiology and Biochemistry, 37(3), 979–990. https://doi.org/10.1159/000430224.CrossRefPubMed

163.

Parissis, J. T., Adamopoulos, S., Venetsanou, K. F., Mentzikof, D. G., Karas, S. M., & Kremastinos, D. T. (2002). Serum profiles of C-C chemokines in acute myocardial infarction: possible implication in postinfarction left ventricular remodeling. Journal of Interferon & Cytokine Research, 22(2), 223–229. https://doi.org/10.1089/107999002753536194.CrossRef

164.

Braunersreuther, V., Montecucco, F., Pelli, G., Galan, K., Proudfoot, A. E., Belin, A., et al. (2013). Treatment with the CC chemokine-binding protein Evasin-4 improves post-infarction myocardial injury and survival in mice. Thrombosis and Haemostasis, 110(4), 807–825. https://doi.org/10.1160/TH13-04-0297.CrossRefPubMed

165.

Liehn, E. A., Merx, M. W., Postea, O., Becher, S., Djalali-Talab, Y., Shagdarsuren, E., et al. (2008). Ccr1 deficiency reduces inflammatory remodelling and preserves left ventricular function after myocardial infarction. Journal of Cellular and Molecular Medicine, 12(2), 496–506. https://doi.org/10.1111/j.1582-4934.2007.00194.x.CrossRefPubMed

166.

Combadiere, C., Ahuja, S. K., Tiffany, H. L., & Murphy, P. M. (1996). Cloning and functional expression of CC CKR5, a human monocyte CC chemokine receptor selective for MIP-1(alpha), MIP-1(beta), and RANTES. Journal of Leukocyte Biology, 60(1), 147–152. https://doi.org/10.1002/jlb.60.1.147.CrossRefPubMed

167.

Dobaczewski, M., Xia, Y., Bujak, M., Gonzalez-Quesada, C., & Frangogiannis, N. G. (2010). CCR5 signaling suppresses inflammation and reduces adverse remodeling of the infarcted heart, mediating recruitment of regulatory T cells. The American Journal of Pathology, 176(5), 2177–2187. https://doi.org/10.2353/ajpath.2010.090759.CrossRefPubMedPubMedCentral

168.

Zamilpa, R., Kanakia, R., Cigarroa, J. t., Dai, Q., Escobar, G. P., Martinez, H., et al. (2011). CC chemokine receptor 5 deletion impairs macrophage activation and induces adverse remodeling following myocardial infarction. American Journal of Physiology. Heart and Circulatory Physiology, 300(4), H1418–H1426. https://doi.org/10.1152/ajpheart.01002.2010.CrossRefPubMedPubMedCentral

169.

Xuan, W., Liao, Y., Chen, B., Huang, Q., Xu, D., Liu, Y., et al. (2011). Detrimental effect of fractalkine on myocardial ischaemia and heart failure. Cardiovascular Research, 92(3), 385–393. https://doi.org/10.1093/cvr/cvr221.CrossRefPubMed

170.

Husberg, C., Nygard, S., Finsen, A. V., Damas, J. K., Frigessi, A., Oie, E., et al. (2008). Cytokine expression profiling of the myocardium reveals a role for CX3CL1 (fractalkine) in heart failure. Journal of Molecular and Cellular Cardiology, 45(2), 261–269.CrossRef

171.

Boag, S. E., Das, R., Shmeleva, E. V., Bagnall, A., Egred, M., Howard, N., et al. (2015). T lymphocytes and fractalkine contribute to myocardial ischemia/reperfusion injury in patients. The Journal of Clinical Investigation, 125(8), 3063–3076. https://doi.org/10.1172/JCI80055.CrossRefPubMedPubMedCentral

172.

Xu, B., Qian, Y., Zhao, Y., Fang, Z., Tang, K., Zhou, N., et al. (2019). Prognostic value of fractalkine/CX3CL1 concentration in patients with acute myocardial infarction treated with primary percutaneous coronary intervention. Cytokine, 113, 365–370. https://doi.org/10.1016/j.cyto.2018.10.006.CrossRefPubMed

173.

Gu, X., Xu, J., Yang, X. P., Peterson, E., & Harding, P. (2015). Fractalkine neutralization improves cardiac function after myocardial infarction. Experimental Physiology, 100(7), 805–817. https://doi.org/10.1113/EP085104.CrossRefPubMedPubMedCentral

174.

Draganova, L., Redgrave, R., Tual-Chalot, S., Marsh, S., Arthur, H., & Spyridopoulos, I. (2019). BS31 The role of fractalkine and CX3CR1-expressing lymphocytes during myocardial ischaemia/reperfusion injury. Heart, 105(Suppl 6), A160–A160. https://doi.org/10.1136/heartjnl-2019-BCS.194.CrossRef

175.

Huang, S., & Frangogiannis, N. G. (2018). Anti-inflammatory therapies in myocardial infarction: failures, hopes and challenges. British Journal of Pharmacology, 175(9), 1377–1400. https://doi.org/10.1111/bph.14155.CrossRefPubMedPubMedCentral

176.

Chung, E. S., Miller, L., Patel, A. N., Anderson, R. D., Mendelsohn, F. O., Traverse, J., et al. (2015). Changes in ventricular remodelling and clinical status during the year following a single administration of stromal cell-derived factor-1 non-viral gene therapy in chronic ischaemic heart failure patients: the STOP-HF randomized phase II trial. European Heart Journal, 36(33), 2228–2238. https://doi.org/10.1093/eurheartj/ehv254.CrossRefPubMedPubMedCentral

177.

Agarwal, U., Ghalayini, W., Dong, F., Weber, K., Zou, Y. R., Rabbany, S. Y., et al. (2010). Role of cardiac myocyte CXCR4 expression in development and left ventricular remodeling after acute myocardial infarction. Circulation Research, 107(5), 667–676. https://doi.org/10.1161/CIRCRESAHA.110.223289.CrossRefPubMedPubMedCentral

178.

Liehn, E. A., Tuchscheerer, N., Kanzler, I., Drechsler, M., Fraemohs, L., Schuh, A., et al. (2011). Double-edged role of the CXCL12/CXCR4 axis in experimental myocardial infarction. Journal of the American College of Cardiology, 58(23), 2415–2423. https://doi.org/10.1016/j.jacc.2011.08.033.CrossRefPubMed

179.

Hayasaki, T., Kaikita, K., Okuma, T., Yamamoto, E., Kuziel, W. A., Ogawa, H., et al. (2006). CC chemokine receptor-2 deficiency attenuates oxidative stress and infarct size caused by myocardial ischemia-reperfusion in mice. Circulation Journal, 70(3), 342–351. https://doi.org/10.1253/circj.70.342.CrossRefPubMed

180.

Hayashidani, S., Tsutsui, H., Shiomi, T., Ikeuchi, M., Matsusaka, H., Suematsu, N., et al. (2003). Anti-monocyte chemoattractant protein-1 gene therapy attenuates left ventricular remodeling and failure after experimental myocardial infarction. Circulation, 108(17), 2134–2140. https://doi.org/10.1161/01.CIR.0000092890.29552.22.CrossRefPubMed

181.

Morimoto, H., Hirose, M., Takahashi, M., Kawaguchi, M., Ise, H., Kolattukudy, P. E., et al. (2008). MCP-1 induces cardioprotection against ischaemia/reperfusion injury: role of reactive oxygen species. Cardiovascular Research, 78(3), 554–562. https://doi.org/10.1093/cvr/cvn035.CrossRefPubMed

182.

Shen, B., Li, J., Gao, L., Zhang, J., & Yang, B. (2013). Role of CC-chemokine receptor 5 on myocardial ischemia-reperfusion injury in rats. Molecular and Cellular Biochemistry, 378(1-2), 137–144. https://doi.org/10.1007/s11010-013-1604-z.CrossRefPubMedPubMedCentral

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