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Calcified Tissue International
Erschienen in: Calcified Tissue International 1/2023

27.05.2023 | Review

Megakaryocyte Secreted Factors Regulate Bone Marrow Niche Cells During Skeletal Homeostasis, Aging, and Disease

verfasst von: Sonali J. Karnik, Murad K. Nazzal, Melissa A. Kacena, Angela Bruzzaniti

Erschienen in: Calcified Tissue International | Ausgabe 1/2023

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Abstract

The bone marrow microenvironment contains a diverse array of cell types under extensive regulatory control and provides for a novel and complex mechanism for bone regulation. Megakaryocytes (MKs) are one such cell type that potentially acts as a master regulator of the bone marrow microenvironment due to its effects on hematopoiesis, osteoblastogenesis, and osteoclastogenesis. While several of these processes are induced/inhibited through MK secreted factors, others are primarily regulated by direct cell–cell contact. Notably, the regulatory effects that MKs exert on these different cell populations has been found to change with aging and disease states. Overall, MKs are a critical component of the bone marrow that should be considered when examining regulation of the skeletal microenvironment. An increased understanding of the role of MKs in these physiological processes may provide insight into novel therapies that can be used to target specific pathways important in hematopoietic and skeletal disorders.
Literatur
1.
Noetzli LJ, French SL, Machlus KR (2019) New insights into the differentiation of megakaryocytes from hematopoietic progenitors. Arterioscler Thromb Vasc Biol 39(7):1288–1300PubMedCentralCrossRefPubMed
2.
3.
4.
Ghosh J et al (2021) Cellular components of the hematopoietic niche and their regulation of hematopoietic stem cell function. Curr Opin Hematol 28(4):243–250PubMedCentralCrossRefPubMed
5.
Taichman RS (2005) Blood and bone: two tissues whose fates are intertwined to create the hematopoietic stem-cell niche. Blood 105(7):2631–2639CrossRefPubMed
6.
Schofield R (1978) The relationship between the spleen colony-forming cell and the haemopoietic stem cell. Blood Cells 4(1–2):7–25PubMed
7.
Heazlewood SY et al (2013) Megakaryocytes co-localise with hemopoietic stem cells and release cytokines that up-regulate stem cell proliferation. Stem Cell Res 11(2):782–792CrossRefPubMed
8.
Grassinger J et al (2010) Phenotypically identical hemopoietic stem cells isolated from different regions of bone marrow have different biologic potential. Blood 116(17):3185–3196CrossRefPubMed
9.
Dominici M et al (2009) Restoration and reversible expansion of the osteoblastic hematopoietic stem cell niche after marrow radioablation. Blood 114(11):2333–2343PubMedCentralCrossRefPubMed
10.
Olson TS et al (2013) Megakaryocytes promote murine osteoblastic HSC niche expansion and stem cell engraftment after radioablative conditioning. Blood 121(26):5238–5249PubMedCentralCrossRefPubMed
11.
Gruzdev GP, Chistopol’skii AS, Suvorova LA (1996) Radiosensitivity and postradiation kinetics of megakaryocyte release of the bone marrow (Analysis based on data of the Chernobyl AES accident sequelae). Radiats Biol Radioecol 36(2):250–263PubMed
12.
Monzen S et al (2009) Radiation sensitivities in the terminal stages of megakaryocytic maturation and platelet production. Radiat Res 172(3):314–320CrossRefPubMed
13.
Caselli A et al (2013) IGF-1-mediated osteoblastic niche expansion enhances long-term hematopoietic stem cell engraftment after murine bone marrow transplantation. Stem Cells 31(10):2193–2204CrossRefPubMed
14.
Wickenhauser C et al (1995) Detection and quantification of transforming growth factor beta (TGF-beta) and platelet-derived growth factor (PDGF) release by normal human megakaryocytes. Leukemia 9(2):310–315PubMed
15.
Demirtas TT et al (2016) Combined delivery of PDGF-BB and BMP-6 for enhanced osteoblastic differentiation. J Mater Sci Mater Med 27(1):12CrossRefPubMed
16.
Antoniades HN (1991) PDGF: a multifunctional growth factor. Baillieres Clin Endocrinol Metab 5(4):595–613CrossRefPubMed
17.
Lambert MP et al (2009) Platelet factor 4 regulates megakaryopoiesis through low-density lipoprotein receptor-related protein 1 (LRP1) on megakaryocytes. Blood 114(11):2290–2298PubMedCentralCrossRefPubMed
18.
Jian J et al (2017) Platelet factor 4 is produced by subsets of myeloid cells in premetastatic lung and inhibits tumor metastasis. Oncotarget 8(17):27725–27739CrossRefPubMed
19.
Lambert MP et al (2015) Intramedullary megakaryocytes internalize released platelet factor 4 and store it in alpha granules. J Thromb Haemost 13(10):1888–1899PubMedCentralCrossRefPubMed
20.
Aidoudi S et al (1996) In vivo effect of platelet factor 4 (PF4) and tetrapeptide AcSDKP on haemopoiesis of mice treated with 5-fluorouracil. Br J Haematol 94(3):443–448CrossRefPubMed
21.
Aidoudi S et al (1997) A 13–24 C-terminal peptide related to PF4 accelerates hematopoietic recovery of progenitor cells in vivo in mice treated with 5-fluorouracil. Int J Hematol 66(4):435–444CrossRefPubMed
22.
Zhao M et al (2014) Megakaryocytes maintain homeostatic quiescence and promote post-injury regeneration of hematopoietic stem cells. Nat Med 20(11):1321–1326CrossRefPubMed
23.
24.
25.
26.
27.
Tie R et al (2019) Interleukin-6 signaling regulates hematopoietic stem cell emergence. Exp Mol Med 51(10):1–12CrossRefPubMed
28.
van Pel M et al (2006) Serpina1 is a potent inhibitor of IL-8-induced hematopoietic stem cell mobilization. Proc Natl Acad Sci U S A 103(5):1469–1474PubMedCentralCrossRefPubMed
29.
Sierra F (2016) Moving geroscience into uncharted waters. J Gerontol A Biol Sci Med Sci 71(11):1385–1387CrossRefPubMed
30.
Poscablo DM et al (2021) Megakaryocyte progenitor cell function is enhanced upon aging despite the functional decline of aged hematopoietic stem cells. Stem Cell Reports 16(6):1598–1613PubMedCentralCrossRefPubMed
31.
Rundberg Nilsson A et al (2016) Human and murine hematopoietic stem cell aging is associated with functional impairments and intrinsic megakaryocytic/erythroid bias. PLoS ONE 11(7):e0158369PubMedCentralCrossRefPubMed
32.
33.
Maryanovich M et al (2018) Adrenergic nerve degeneration in bone marrow drives aging of the hematopoietic stem cell niche. Nat Med 24(6):782–791PubMedCentralCrossRefPubMed
34.
35.
Fishley B, Alexander WS (2004) Thrombopoietin signalling in physiology and disease. Growth Factors 22(3):151–155CrossRefPubMed
36.
37.
38.
39.
Li L et al (2022) Insights into regulatory factors in megakaryocyte development and function: basic mechanisms and potential targets. Front Biosci (Landmark Ed) 27(11):313CrossRefPubMed
40.
Yan XQ et al (1996) A model of myelofibrosis and osteosclerosis in mice induced by overexpressing thrombopoietin (mpl ligand): reversal of disease by bone marrow transplantation. Blood 88(2):402–409CrossRefPubMed
41.
Villeval JL et al (1997) High thrombopoietin production by hematopoietic cells induces a fatal myeloproliferative syndrome in mice. Blood 90(11):4369–4383CrossRefPubMed
42.
Kakumitsu H et al (2005) Transgenic mice overexpressing murine thrombopoietin develop myelofibrosis and osteosclerosis. Leuk Res 29(7):761–769CrossRefPubMed
43.
Olivos DJ 3rd et al (2017) Lnk deficiency leads to TPO-mediated osteoclastogenesis and increased bone mass phenotype. J Cell Biochem 118(8):2231–2240PubMedCentralCrossRefPubMed
44.
Bord S et al (2000) Megakaryocyte population in human bone marrow increases with estrogen treatment: a role in bone remodeling? Bone 27(3):397–401CrossRefPubMed
45.
46.
Kacena MA et al (2004) Megakaryocyte-osteoblast interaction revealed in mice deficient in transcription factors GATA-1 and NF-E2. J Bone Miner Res 19(4):652–660CrossRefPubMed
47.
Meijome TE et al (2016) C-Mpl Is expressed on osteoblasts and osteoclasts and is important in regulating skeletal homeostasis. J Cell Biochem 117(4):959–969CrossRefPubMed
48.
49.
Shivdasani RA et al (1995) Transcription factor NF-E2 is required for platelet formation independent of the actions of thrombopoietin/MGDF in megakaryocyte development. Cell 81(5):695–704CrossRefPubMed
50.
Vyas P et al (1999) Consequences of GATA-1 deficiency in megakaryocytes and platelets. Blood 93(9):2867–2875CrossRefPubMed
51.
Kacena MA et al (2013) The effects of GATA-1 and NF-E2 deficiency on bone biomechanical, biochemical, and mineral properties. J Cell Physiol 228(7):1594–1600PubMedCentralCrossRefPubMed
52.
Miao D et al (2004) Megakaryocyte-bone marrow stromal cell aggregates demonstrate increased colony formation and alkaline phosphatase expression in vitro. Tissue Eng 10(5–6):807–817CrossRefPubMed
53.
Ciovacco WA et al (2010) Immature and mature megakaryocytes enhance osteoblast proliferation and inhibit osteoclast formation. J Cell Biochem 109(4):774–781PubMedCentralPubMed
54.
Maupin KA et al (2019) Aging negatively impacts the ability of megakaryocytes to stimulate osteoblast proliferation and bone mass. Bone 127:452–459PubMedCentralCrossRefPubMed
55.
56.
Ciovacco WA et al (2009) The role of gap junctions in megakaryocyte-mediated osteoblast proliferation and differentiation. Bone 44(1):80–86CrossRefPubMed
57.
Lemieux JM, Horowitz MC, Kacena MA (2010) Involvement of integrins alpha(3)beta(1) and alpha(5)beta(1) and glycoprotein IIb in megakaryocyte-induced osteoblast proliferation. J Cell Biochem 109(5):927–932PubMedCentralPubMed
58.
Tang Y et al (2020) Megakaryocytes promote bone formation through coupling osteogenesis with angiogenesis by secreting TGF-beta1. Theranostics 10(5):2229–2242PubMedCentralCrossRefPubMed
59.
Martelli F et al (2009) Removal of the spleen in mice alters the cytokine expression profile of the marrow micro-environment and increases bone formation. Ann N Y Acad Sci 1176:77–86PubMedCentralCrossRefPubMed
60.
Robey PG et al (1987) Osteoblasts synthesize and respond to transforming growth factor-type beta (TGF-beta) in vitro. J Cell Biol 105(1):457–463CrossRefPubMed
61.
Bonewald LF, Dallas SL (1994) Role of active and latent transforming growth factor beta in bone formation. J Cell Biochem 55(3):350–357CrossRefPubMed
62.
Jilka RL et al (1998) Osteoblast programmed cell death (apoptosis): modulation by growth factors and cytokines. J Bone Miner Res 13(5):793–802CrossRefPubMed
63.
Alliston T et al (2001) TGF-beta-induced repression of CBFA1 by Smad3 decreases cbfa1 and osteocalcin expression and inhibits osteoblast differentiation. EMBO J 20(9):2254–2272PubMedCentralCrossRefPubMed
64.
Kassem M, Kveiborg M, Eriksen EF (2000) Production and action of transforming growth factor-beta in human osteoblast cultures: dependence on cell differentiation and modulation by calcitriol. Eur J Clin Invest 30(5):429–437CrossRefPubMed
65.
Ciaffoni F et al (2015) Activation of non-canonical TGF-beta1 signaling indicates an autoimmune mechanism for bone marrow fibrosis in primary myelofibrosis. Blood Cells Mol Dis 54(3):234–241PubMedCentralCrossRefPubMed
66.
Sipe JB et al (2004) Localization of bone morphogenetic proteins (BMPs)-2, -4, and -6 within megakaryocytes and platelets. Bone 35(6):1316–1322CrossRefPubMed
67.
Garimella R et al (2007) Expression of bone morphogenetic proteins and their receptors in the bone marrow megakaryocytes of GATA-1(low) mice: a possible role in osteosclerosis. J Histochem Cytochem 55(7):745–752CrossRefPubMed
68.
Bock O et al (2008) Bone morphogenetic proteins are overexpressed in the bone marrow of primary myelofibrosis and are apparently induced by fibrogenic cytokines. Am J Pathol 172(4):951–960PubMedCentralCrossRefPubMed
69.
70.
Spinella-Jaegle S et al (2001) Opposite effects of bone morphogenetic protein-2 and transforming growth factor-beta1 on osteoblast differentiation. Bone 29(4):323–330CrossRefPubMed
71.
72.
Ikeda E et al (1988) Effect of interleukin 1 beta on osteoblastic clone MC3T3-E1 cells. Calcif Tissue Int 43(3):162–166CrossRefPubMed
73.
Jiang S et al (1994) Cytokine production by primary bone marrow megakaryocytes. Blood 84(12):4151–4156CrossRefPubMed
74.
Wickenhauser C et al (1995) Secretion of cytokines (interleukins-1 alpha, -3, and -6 and granulocyte-macrophage colony-stimulating factor) by normal human bone marrow megakaryocytes. Blood 85(3):685–691CrossRefPubMed
75.
Wang T, He C (2020) TNF-alpha and IL-6: the link between immune and bone system. Curr Drug Targets 21(3):213–227PubMed
76.
Winter O et al (2010) Megakaryocytes constitute a functional component of a plasma cell niche in the bone marrow. Blood 116(11):1867–1875CrossRefPubMed
77.
Tatakis DN (1992) Human platelet factor 4 is a direct inhibitor of human osteoblast-like osteosarcoma cell growth. Biochem Biophys Res Commun 187(1):287–293CrossRefPubMed
78.
Kohler A et al (2011) G-CSF-mediated thrombopoietin release triggers neutrophil motility and mobilization from bone marrow via induction of Cxcr2 ligands. Blood 117(16):4349–4357PubMedCentralCrossRefPubMed
79.
80.
Huang H, Ma L, Kyrkanides S (2016) Effects of vascular endothelial growth factor on osteoblasts and osteoclasts. Am J Orthod Dentofacial Orthop 149(3):366–373CrossRefPubMed
81.
Knaup I et al (2022) Impact of FGF1 on human periodontal ligament fibroblast growth, osteogenic differentiation and inflammatory reaction in vitro. J Orofac Orthop 83(Suppl 1):42–55CrossRefPubMed
82.
Yang X et al (2006) Sprouty genes are expressed in osteoblasts and inhibit fibroblast growth factor-mediated osteoblast responses. Calcif Tissue Int 78(4):233–240CrossRefPubMed
83.
Breton-Gorius J et al (1992) Localization of platelet osteonectin at the internal face of the alpha-granule membranes in platelets and megakaryocytes. Blood 79(4):936–941CrossRefPubMed
84.
Murate T et al (1997) The production of tissue inhibitors of metalloproteinases (TIMPs) in megakaryopoiesis: possible role of platelet- and megakaryocyte-derived TIMPs in bone marrow fibrosis. Br J Haematol 99(1):181–189CrossRefPubMed
85.
Tiedemann K, Tsao S, Komarova SV (2022) Platelets and osteoblasts: secretome connections. Am J Physiol Cell Physiol 323(2):C347–C353CrossRefPubMed
86.
87.
Delany AM, Amling M, Priemel M, Howe C, Baron R, Canalis E (2000) Osteopenia and decreased bone formation in osteonectin-deficient mice. J Clin Invest. 105(7):915–923. https://​doi.​org/​10.​1172/​JCI7039. Erratum in: J Clin Invest 2000 May;105(9):1325. PMID: 10749571; PMCID: PMC377474
88.
89.
90.
Jeanneau C, Sultan Y (1988) Tissue plasminogen activator in human megakaryocytes and platelets: immunocytochemical localization, immunoblotting and zymographic analysis. Thromb Haemost 59(3):529–534CrossRefPubMed
91.
Daci E et al (2003) Increased bone formation in mice lacking plasminogen activators. J Bone Miner Res 18(7):1167–1176CrossRefPubMed
92.
93.
Gazit D et al (1998) Bone loss (osteopenia) in old male mice results from diminished activity and availability of TGF-beta. J Cell Biochem 70(4):478–488CrossRefPubMed
94.
Thiede MA et al (1994) Presence of messenger ribonucleic acid encoding osteocalcin, a marker of bone turnover, in bone marrow megakaryocytes and peripheral blood platelets. Endocrinology 135(3):929–937CrossRefPubMed
95.
Bord S et al (2004) Synthesis of osteoprotegerin and RANKL by megakaryocytes is modulated by oestrogen. Br J Haematol 126(2):244–251CrossRefPubMed
96.
Kartsogiannis V et al (1999) Localization of RANKL (receptor activator of NF kappa B ligand) mRNA and protein in skeletal and extraskeletal tissues. Bone 25(5):525–534CrossRefPubMed
97.
Chagraoui H et al (2003) Expression of osteoprotegerin mRNA and protein in murine megakaryocytes. Exp Hematol 31(11):1081–1088CrossRefPubMed
98.
Bord S et al (2005) Megakaryocytes modulate osteoblast synthesis of type-l collagen, osteoprotegerin, and RANKL. Bone 36(5):812–819CrossRefPubMed
99.
Beeton CA et al (2006) Osteoclast formation and bone resorption are inhibited by megakaryocytes. Bone 39(5):985–990CrossRefPubMed
100.
Kacena MA et al (2006) Megakaryocyte-mediated inhibition of osteoclast development. Bone 39(5):991–999CrossRefPubMed
101.
Woolthuis CM, de Haan G, Huls G (2011) Aging of hematopoietic stem cells: Intrinsic changes or micro-environmental effects? Curr Opin Immunol 23(4):512–517CrossRefPubMed
102.
103.
Kacena MA, Ciovacco WA (2010) Megakaryocyte-bone cell interactions. Adv Exp Med Biol 658:31–41CrossRefPubMed
104.
Kanagasabapathy D et al (2020) Megakaryocytes promote osteoclastogenesis in aging. Aging (Albany NY) 12(14):15121–15133CrossRefPubMed
105.
Lovibond AC et al (2003) TGF-beta-induced SOCS3 expression augments TNF-alpha-induced osteoclast formation. Biochem Biophys Res Commun 309(4):762–767CrossRefPubMed
106.
107.
108.
109.
Suva LJ, Hartman E, Dilley JD, Russell S, Akel NS, Skinner RA, Hogue WR, Budde U, Varughese KI, Kanaji T, Ware J (2008) Platelet dysfunction and a high bone mass phenotype in a murine model of platelet-type von Willebrand disease. Am J Pathol 172(2):430–439. https://​doi.​org/​10.​2353/​ajpath.​2008.​070417
110.
Mohle R et al (1997) Constitutive production and thrombin-induced release of vascular endothelial growth factor by human megakaryocytes and platelets. Proc Natl Acad Sci U S A 94(2):663–668PubMedCentralCrossRefPubMed
111.
Hong MH et al (2000) The inhibitory effect of interleukin-10 on mouse osteoclast formation involves novel tyrosine-phosphorylated proteins. J Bone Miner Res 15(5):911–918CrossRefPubMed
112.
Liu D, Yao S, Wise GE (2006) Effect of interleukin-10 on gene expression of osteoclastogenic regulatory molecules in the rat dental follicle. Eur J Oral Sci 114(1):42–49CrossRefPubMed
113.
114.
115.
Carmody EE et al (2002) Viral interleukin-10 gene inhibition of inflammation, osteoclastogenesis, and bone resorption in response to titanium particles. Arthritis Rheum 46(5):1298–1308CrossRefPubMed
116.
117.
Fazzalari NL et al (2001) The ratio of messenger RNA levels of receptor activator of nuclear factor kappaB ligand to osteoprotegerin correlates with bone remodeling indices in normal human cancellous bone but not in osteoarthritis. J Bone Miner Res 16(6):1015–1027CrossRefPubMed
118.
Cao J et al (2003) Expression of RANKL and OPG correlates with age-related bone loss in male C57BL/6 mice. J Bone Miner Res 18(2):270–277CrossRefPubMed
119.
Cao JJ et al (2005) Aging increases stromal/osteoblastic cell-induced osteoclastogenesis and alters the osteoclast precursor pool in the mouse. J Bone Miner Res 20(9):1659–1668CrossRefPubMed
120.
121.
Rokkam VR, K.R., Secondary Thrombocytosis. 2022, Treasure Island (FL): StatPearls Publishing.
122.
Kacena MA, Horowitz MC (2006) The role of megakaryocytes in skeletal homeostasis and rheumatoid arthritis. Curr Opin Rheumatol 18(4):405–410CrossRefPubMed
123.
124.
Wang Y et al (2022) Rheumatoid arthritis, systemic lupus erythematosus and primary Sjögren’s syndrome shared megakaryocyte expansion in peripheral blood. Ann Rheum Dis 81(3):379–385CrossRefPubMed
125.
Narducci P, Bareggi R, Nicolin V (2011) Receptor activator for nuclear factor kappa B ligand (RANKL) as an osteoimmune key regulator in bone physiology and pathology. Acta Histochem 113(2):73–81CrossRefPubMed
126.
Sarzi-Puttini P et al (2005) Osteoarthritis: an overview of the disease and its treatment strategies. Semin Arthritis Rheum 35(1 Suppl 1):1–10CrossRefPubMed
127.
Burr DB, Gallant MA (2012) Bone remodelling in osteoarthritis. Nat Rev Rheumatol 8(11):665–673CrossRefPubMed
128.
Lorenz H, Richter W (2006) Osteoarthritis: cellular and molecular changes in degenerating cartilage. Prog Histochem Cytochem 40(3):135–163CrossRefPubMed
129.
Kapoor M et al (2011) Role of proinflammatory cytokines in the pathophysiology of osteoarthritis. Nat Rev Rheumatol 7(1):33–42CrossRefPubMed
130.
Rhodes M (2022) Hematopoietic elements in osteoarthritic femurs compared to normal bone marrow as evaluated by immunohistochemistry. Biomed J Sci Tech Res 44(2):35300–35305
131.
Zhang J et al (2019) CD226 is involved in megakaryocyte activation and early-stage differentiation. Mol Immunol 107:123–131CrossRefPubMed
132.
Zhang J et al (2020) Deficiency of platelet adhesion molecule CD226 causes megakaryocyte development and platelet hyperactivity. FASEB J 34(5):6871–6887CrossRefPubMed
133.
134.
Liu Y et al (2021) CD226 Is required to maintain megakaryocytes/platelets homeostasis in the treatment of knee osteoarthritis with platelet-rich plasma in mice. Front Pharmacol 12:732453PubMedCentralCrossRefPubMed
135.
Pillai NR, Aggarwal A, Orchard P (2022) Phenotype-autosomal recessive osteopetrosis. Bone 165:116577CrossRefPubMed
136.
137.
138.
139.
Yorgan T et al (2018) The high bone mass phenotype of Lrp5-mutant mice is not affected by megakaryocyte depletion. Biochem Biophys Res Commun 497(2):659–666CrossRefPubMed
140.
141.
Stavnichuk M et al (2021) Severity of megakaryocyte-driven osteosclerosis in Mpig6b-deficient mice is sex-linked. J Bone Miner Res 36(4):803–813CrossRefPubMed
142.
143.
Tella SH, Gallagher JC (2014) Prevention and treatment of postmenopausal osteoporosis. J Steroid Biochem Mol Biol 142:155–170CrossRefPubMed
144.
Fischer V, Haffner-Luntzer M (2022) Interaction between bone and immune cells: implications for postmenopausal osteoporosis. Semin Cell Dev Biol 123:14–21CrossRefPubMed
145.
Metadaten
Titel
Megakaryocyte Secreted Factors Regulate Bone Marrow Niche Cells During Skeletal Homeostasis, Aging, and Disease
verfasst von
Sonali J. Karnik
Murad K. Nazzal
Melissa A. Kacena
Angela Bruzzaniti
Publikationsdatum
27.05.2023
Verlag
Springer US
Erschienen in
Calcified Tissue International / Ausgabe 1/2023
Print ISSN: 0171-967X
Elektronische ISSN: 1432-0827
DOI
https://doi.org/10.1007/s00223-023-01095-y

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