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Journal of Cardiovascular Translational Research

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29.02.2016 | Original Article

Caspase-1 Plays a Critical Role in Accelerating Chronic Kidney Disease-Promoted Neointimal Hyperplasia in the Carotid Artery

verfasst von: Lucas M. Ferrer, Alexandra M. Monroy, Jahaira Lopez-Pastrana, Gayani Nanayakkara, Ramon Cueto, Ya-feng Li, Xinyuan Li, Hong Wang, Xiao-feng Yang, Eric T. Choi

Erschienen in: Journal of Cardiovascular Translational Research | Ausgabe 2/2016

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Abstract

To determine whether caspase-1 is critical in chronic kidney disease (CKD)-mediated arterial neointimal hyperplasia (NH), we utilized caspase^−/− mice and induced NH in carotid artery in a CKD environment, and uremic sera-stimulated human vascular smooth muscle cells (VSMC). We made the following findings: (1) Caspase-1 inhibition corrected uremic sera-mediated downregulation of VSMC contractile markers, (2) CKD-promoted NH was attenuated in caspase^−/− mice, (3) CKD-mediated downregulation of contractile markers was rescued in caspase null mice, and (4) expression of VSMC migration molecule αvβ3 integrin was reduced in caspase^−/− tissues. Our results suggested that caspase-1 pathway senses CKD metabolic danger signals. Further, CKD-mediated increase of contractile markers in VSMC and increased expression of VSMC migration molecule αvβ3 integrin in NH formation were caspase-1 dependent. Therefore, caspase-1 is a novel therapeutic target for the suppression of CKD-promoted NH.

Levey, A. S., Coresh, J., Balk, E., Kausz, A. T., Levin, A., Steffes, M. W., et al. (2003). National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Annals of Internal Medicine, 139(2), 137–147. Guideline Practice Guideline Research Support, Non-U.S. Gov’t. CrossRefPubMed

Basnakian, A. G., Shah, S. V., Ok, E., Altunel, E., & Apostolov, E. O. (2010). Carbamylated LDL. Advances in Clinical Chemistry, 51, 25–52.CrossRefPubMed

Foundation, N. K. (2002). K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. American Journal of Kidney Diseases, 39(2 Suppl 1), S1–266. Guideline Practice Guideline.

Moradi, H., Sica, D. A., & Kalantar-Zadeh, K. (2013). Cardiovascular burden associated with uremic toxins in patients with chronic kidney disease. American Journal of Nephrology, 38(2), 136–148. doi:10.1159/000351758. Research Support, N.I.H., Extramural Review.CrossRefPubMed

Feldman, H. I., Kobrin, S., & Wasserstein, A. (1996). Hemodialysis vascular access morbidity. Journal of the American Society of Nephrology, 7(4), 523–535. Editorial Research Support, U.S. Gov’t, Non-P.H.S. Review.PubMed

Go, A. S., Chertow, G. M., Fan, D., McCulloch, C. E., & Hsu, C. Y. (2004). Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization. New England Journal of Medicine, 351(13), 1296–1305. doi:10.1056/NEJMoa041031.CrossRefPubMed

Daniels, S. E., Beineke, P., Rhees, B., McPherson, J. A., Kraus, W. E., Thomas, G. S., et al. (2014). Biological and analytical stability of a peripheral blood gene expression score for obstructive coronary artery disease in the PREDICT and COMPASS studies. Journal of Cardiovascular Translational Research, 7(7), 615–622. doi:10.1007/s12265-014-9583-3. Research Support, Non-U.S. Gov’t Validation Studies.CrossRefPubMedPubMedCentral

Fernandez-Friera, L., Ibanez, B., & Fuster, V. (2014). Imaging subclinical atherosclerosis: is it ready for prime time? A review. Journal of Cardiovascular Translational Research, 7(7), 623–634. doi:10.1007/s12265-014-9582-4.CrossRefPubMed

Wasse, H., Huang, R., Naqvi, N., Smith, E., Wang, D., & Husain, A. (2012). Inflammation, oxidation and venous neointimal hyperplasia precede vascular injury from AVF creation in CKD patients. The Journal of Vascular Access, 13(2), 168–174. doi:10.5301/jva.5000024.CrossRefPubMedPubMedCentral

10.

Langer, S., Kokozidou, M., Heiss, C., Kranz, J., Kessler, T., Paulus, N., et al. (2010). Chronic kidney disease aggravates arteriovenous fistula damage in rats. Kidney International, 78(12), 1312–1321. doi:10.1038/ki.2010.353. Research Support, Non-U.S. Gov’t.CrossRefPubMed

11.

Kokubo, T., Ishikawa, N., Uchida, H., Chasnoff, S. E., Xie, X., Mathew, S., et al. (2009). CKD accelerates development of neointimal hyperplasia in arteriovenous fistulas. Journal of the American Society of Nephrology, 20(6), 1236–1245. doi:10.1681/ASN.2007121312. Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov’t.CrossRefPubMedPubMedCentral

12.

Kim, D. N., Schmee, J., Lee, K. T., & Thomas, W. A. (1987). Atherosclerotic lesions in the coronary arteries of hyperlipidemic swine. part 1. Cell increases, divisions, losses and cells of origin in first 90 days on diet. Atherosclerosis, 64(2–3), 231–242.CrossRefPubMed

13.

Schwartz, S. M., deBlois, D., & O’Brien, E. R. (1995). The intima. Soil for atherosclerosis and restenosis. Circulation Research, 77(3), 445–465.CrossRefPubMed

14.

Stary, H. C., Blankenhorn, D. H., Chandler, A. B., Glagov, S., Insull, W., Jr., Richardson, M., et al. (1992). A definition of the intima of human arteries and of its atherosclerosis-prone regions. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis. American Heart Association. Arteriosclerical Thrombone, 12(1), 120–134.

15.

Virmani, R., Kolodgie, F. D., Burke, A. P., Farb, A., & Schwartz, S. M. (2000). Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arteriosclerosis, Thrombosis, and Vascular Biology, 20(5), 1262–1275.CrossRefPubMed

16.

Alexander, M. R., & Owens, G. K. (2012). Epigenetic control of smooth muscle cell differentiation and phenotypic switching in vascular development and disease. Annual Review of Physiology, 74, 13–40. doi:10.1146/annurev-physiol-012110-142315.CrossRefPubMed

17.

Monroy, M. A., Fang, J, Li, S, Ferrer, L, Birkenbach, M. P., Lee et al. (2014). Chronic kidney disease alters vascular smooth muscle cell phenotype. Frontiers in Bioscience (Landmark Edition) in press.

18.

Regan, C. P., Adam, P. J., Madsen, C. S., & Owens, G. K. (2000). Molecular mechanisms of decreased smooth muscle differentiation marker expression after vascular injury. Journal of Clinical Investigation, 106(9), 1139–1147. doi:10.1172/JCI10522. Research Support, Non-U.S. Gov’t Research Support, U.S. Gov’t, P.H.S. CrossRefPubMedPubMedCentral

19.

Owens, G. K., Kumar, M. S., & Wamhoff, B. R. (2004). Molecular regulation of vascular smooth muscle cell differentiation in development and disease. Physiological Reviews, 84(3), 767–801. doi:10.1152/physrev.00041.2003. Research Support, Non-U.S. Gov’t Research Support, U.S. Gov’t, P.H.S. Review.CrossRefPubMed

20.

Yin, Y., Yan, Y., Jiang, X., Mai, J., Chen, N. C., Wang, H., et al. (2009). Inflammasomes are differentially expressed in cardiovascular and other tissues. International Journal of Immunopathology and Pharmacology, 22(2), 311–322.PubMedPubMedCentral

21.

Yin, Y., Pastrana, J. L., Li, X., Huang, X., Mallilankaraman, K., Choi, E. T., et al. (2013). Inflammasomes: sensors of metabolic stresses for vascular inflammation. Frontiers in Bioscience, 18, 638–649. Research Support, N.I.H., Extramural.CrossRef

22.

Yin, Y., Li, X., Sha, X., Xi, H., Li, Y. F., Shao, Y., et al. (2015). Early hyperlipidemia promotes endothelial activation via a caspase-1-sirtuin 1 pathway. Arteriosclerosis, Thrombosis, and Vascular Biology, 35(4), 804–816. doi:10.1161/ATVBAHA.115.305282.CrossRefPubMedPubMedCentral

23.

Shen, J., Yin, Y., Mai, J., Xiong, X., Pansuria, M., Liu, J., et al. (2010). Caspase-1 recognizes extended cleavage sites in its natural substrates. Atherosclerosis, 210(2), 422–429. doi:10.1016/j.atherosclerosis.2009.12.017.CrossRefPubMedPubMedCentral

24.

Lopez-Pastrana, J., Ferrer, L. M., Li, Y. F., Xiong, X., Xi, H., Cueto, R., et al. (2015). Inhibition of caspase-1 activation in endothelial cells improves angiogenesis: a novel therapeutic potential for ischemia. Journal of Biological Chemistry, 290(28), 17485–17494. doi:10.1074/jbc.M115.641191.CrossRefPubMed

25.

Li, Y. F., Huang, X., Li, X., Gong, R., Yin, Y., Nelson, J., et al. (2016). Caspase-1 mediates hyperlipidemia-weakened progenitor cell vessel repair. Front Bioscience (Landmark Ed), 21, 178–191.CrossRef

26.

Monroy, M. A., Fang, J., Li, S., Ferrer, L., Birkenbach, M. P., Lee, I. J., et al. (2015). Chronic kidney disease alters vascular smooth muscle cell phenotype. Front Bioscience (Landmark Ed), 20, 784–795.CrossRef

27.

Anders, H. J., & Muruve, D. A. (2011). The inflammasomes in kidney disease. Journal of the American Society of Nephrology, 22(6), 1007–1018. doi:10.1681/ASN.2010080798. Research Support, Non-U.S. Gov’t Review.CrossRefPubMed

28.

Kumar, A., Hoover, J. L., Simmons, C. A., Lindner, V., & Shebuski, R. J. (1997). Remodeling and neointimal formation in the carotid artery of normal and P-selectin-deficient mice. Circulation, 96(12), 4333–4342.CrossRefPubMed

29.

Kuida, K., Lippke, J. A., Ku, G., Harding, M. W., Livingston, D. J., Su, M. S., et al. (1995). Altered cytokine export and apoptosis in mice deficient in interleukin-1 beta converting enzyme. Science, 267(5206), 2000–2003. Research Support, Non-U.S. Gov’t.CrossRefPubMed

30.

Lee, I. J., Hilliard, B., Swami, A., Madara, J. C., Rao, S., Patel, T., et al. (2012). Growth arrest-specific gene 6 (Gas6) levels are elevated in patients with chronic renal failure. Nephrology, Dialysis, Transplantation, 27(11), 4166–4172. doi:10.1093/ndt/gfs337. Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov’t.CrossRefPubMedPubMedCentral

31.

Eddy, A. A., Lopez-Guisa, J. M., Okamura, D. M., & Yamaguchi, I. (2012). Investigating mechanisms of chronic kidney disease in mouse models. Pediatric Nephrology, 27(8), 1233–1247. doi:10.1007/s00467-011-1938-2. Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov’t Review.CrossRefPubMedPubMedCentral

32.

Lichtnekert, J., Kulkarni, O. P., Mulay, S. R., Rupanagudi, K. V., Ryu, M., & Allam, R. (2011). Anti-GBM glomerulonephritis involves IL-1 but is independent of NLRP3/ASC inflammasome-mediated activation of caspase-1. PLoS ONE, 6(10), e26778. doi:10.1371/journal.pone.0026778. Research Support, Non-U.S. Gov’t.CrossRefPubMedPubMedCentral

33.

Kokubo, T., Uchida, H., & Choi, E. T. (2007). Integrin alpha(v)beta(3) as a target in the prevention of neointimal hyperplasia. Journal of Vascular Surgery, 45(Suppl A), A33–38. doi:10.1016/j.jvs.2007.02.069. Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov’t Review.CrossRefPubMed

34.

Desgrosellier, J. S., & Cheresh, D. A. (2010). Integrins in cancer: biological implications and therapeutic opportunities. Nature Reviews Cancer, 10(1), 9–22. doi:10.1038/nrc2748. Research Support, N.I.H., Extramural Review.CrossRefPubMedPubMedCentral

35.

Lee, T., & Roy-Chaudhury, P. (2009). Advances and new frontiers in the pathophysiology of venous neointimal hyperplasia and dialysis access stenosis. Advances in Chronic Kidney Disease, 16(5), 329–338. doi:10.1053/j.ackd.2009.06.009. Research Support, N.I.H., Extramural Research Support, U.S. Gov’t, Non-P.H.S. Review.CrossRefPubMedPubMedCentral

36.

Lee, H., Manns, B., Taub, K., Ghali, W. A., Dean, S., Johnson, D., et al. (2002). Cost analysis of ongoing care of patients with end-stage renal disease: the impact of dialysis modality and dialysis access. American Journal of Kidney Diseases, 40(3), 611–622. doi:10.1053/ajkd.2002.34924. Comparative Study Research Support, Non-U.S. Gov’t.CrossRefPubMed

37.

Yajima, N., Takahashi, M., Morimoto, H., Shiba, Y., Takahashi, Y., Masumoto, J., et al. (2008). Critical role of bone marrow apoptosis-associated speck-like protein, an inflammasome adaptor molecule, in neointimal formation after vascular injury in mice. Circulation, 117(24), 3079–3087.CrossRefPubMed

38.

Villegas, L. R., Kluck, D., Field, C., Oberley-Deegan, R. E., Woods, C., Yeager, M. E., et al. (2013). Superoxide dismutase mimetic, MnTE-2-PyP, attenuates chronic hypoxia-induced pulmonary hypertension, pulmonary vascular remodeling, and activation of the NALP3 inflammasome. Antioxidants and Redox Signaling, 18(14), 1753–1764. doi:10.1089/ars.2012.4799. Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov’t.CrossRefPubMedPubMedCentral

39.

Duewell, P., Kono, H., Rayner, K. J., Sirois, C. M., Vladimer, G., Bauernfeind, F. G., et al. (2010). NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals. Nature, 464(7293), 1357–1361. doi:10.1038/nature08938. Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov’t.CrossRefPubMedPubMedCentral

40.

Usui, F., Shirasuna, K., Kimura, H., Tatsumi, K., Kawashima, A., Karasawa, T., et al. (2012). Critical role of caspase-1 in vascular inflammation and development of atherosclerosis in Western diet-fed apolipoprotein E-deficient mice. Biochemical and Biophysical Research Communications, 425(2), 162–168. doi:10.1016/j.bbrc.2012.07.058. Research Support, Non-U.S. Gov’t.CrossRefPubMed

Titel: Caspase-1 Plays a Critical Role in Accelerating Chronic Kidney Disease-Promoted Neointimal Hyperplasia in the Carotid Artery
verfasst von: Lucas M. Ferrer
Alexandra M. Monroy
Jahaira Lopez-Pastrana
Gayani Nanayakkara
Ramon Cueto
Ya-feng Li
Xinyuan Li
Hong Wang
Xiao-feng Yang
Eric T. Choi
Publikationsdatum: 29.02.2016
Verlag: Springer US
Erschienen in: Journal of Cardiovascular Translational Research / Ausgabe 2/2016
Print ISSN: 1937-5387
Elektronische ISSN: 1937-5395
DOI: https://doi.org/10.1007/s12265-016-9683-3

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Caspase-1 Plays a Critical Role in Accelerating Chronic Kidney Disease-Promoted Neointimal Hyperplasia in the Carotid Artery

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