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Research Article

Cartilage Formation and Calcification in Arteries of Mice Lacking Matrix Gla Protein

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Pages 272-278 | Published online: 06 Aug 2009

References

  • Giachelli, C.M. (1999). Ectopic calcification: Gathering hard facts about soft tissue mineralization. Am. J. Pathol. 154:671–675.
  • Giachelli, C.M. (2001). Ectopic calcification: New concepts in cellular regulation. Z. Kardiol. 90 (suppl. 3):III/631–III/37.
  • Wallin, R., Wajih, N., Greenwood, G.T., and Sane, D.C. (2001). Arterial calcification: A review of mechanisms, animal models, and the prospects for therapy. Med. Res. Rev. 21:274–301.
  • Janzen, J., and Vuong, P.N. (2001). Arterial calcifications: Morphological aspects and their pathological implications. Z. Kardiol. 90 (suppl. 3):III/6– III/11.
  • Proudfoot, D., and Shanahan, C.M. (2001). Biology of calcification in vascular cells: Intima versus media. Herz 26:245–251.
  • Luo, G., Ducy, P., McKee, M.D., Pinero, G.J., Loyer, E., Behringer, R.R., and Karsenty, G. (1997). Spontaneous calcification of arteries and cartilage in mice lacking matrix Gla protein. Nature 386:78–81.
  • Langelier, E., Suetterlin, R., Hoemann, C.D., Aebi, U., and Buschmann, M.D. (2000). The chondrocyte cytoskeleton in mature articular cartilage: Structure and distribution of actin, tubulin, and vimentin filaments. J. His- tochem. Cytochem. 48:1307–1320.
  • Poole, A.R., Reddi, A.H., and Rosenberg, L.C. (1982). Persistence of car- tilage proteoglycan and link protein during matrix-induced endochondral bone development: An immunofluorescent study. Dev. Biol. 2:532–539.
  • Caterson, B., Baker, J.R., Christner, J.E., Lee, Y., and Lentz, M. (1985). Monoclonal antibodies as probes for determining the microheterogeneity of the link proteins of cartilage proteoglycan. J. Biol. Chem. 20:11348–11356.
  • Canfield, A.E., Doherty, M.J., Wood, A.C., Farrington, C., Ashton, B., Begum, N., Harvey, B., Poole, A., Grant, M.E., and Boot-Handford, R.P. (2000). Role of pericytes in vascular calcification. Z. Kardiol. 89 (suppl. 3): II/20–II/27.
  • Qiao, J.-H., Fishbein, M.C., Demer, L.L., and Lusis, A.J. (1995). Genetic determination of cartilaginous metaplasia in mouse aorta. Arterioscler. Thromb. Vasc. Biol. 15:2265–2272.
  • Deneke, T., Langer, K., Grewe, P.H., Harrer, E., and Mu¨ller, K.-M. (2001). Ossification in atherosclerotic carotid arteries. Z. Kardiol. 90 (suppl. 3): III/106–III/115.
  • Jeziorska, M., McCollum, C., and Woolley, D.E. (1998). Observations on bone formation and remodeling in advanced atherosclerotic lesions of human carotid arteries. Virchows Arch. 433:559–565.
  • Jeziorska, M. (2001). Transforming growth factor-ßs and CD105 expres- sion in calcification and bone formation in human atherosclerotic lesions. Z. Kardiol. 90 (suppl. 3):III/23–III/26.
  • Karsenty, G. (2001). Chondrogenesis just ain’t what it used to be. J. Clin. Invest. 107:405–407.
  • Bi, W., Deng, J.M., Zhang, Z., Behringer, R.R., and de Crombrugghe, B. (1999). Sox9 is required for cartilage formation. Nat. Genet. 22:85–89.
  • Cancedda, R., Castagnola, P., Cancedda, F.D., Dozin, B., and Quatro, R. (2000). Developmental control of chondrogenesis and osteogenesis. Int. J. Dev. Biol. 44:707–714.
  • Upholt, W.P., and Olsen, B.R. (1991). The active genes of cartilage. In Cartilage: Molecular Aspects, B. Hall and S. Newman (eds.), pp. 1–57. (CRC Press, Boca Raton, FL).
  • Olsen, B.R., Reginato, A.M., and Wang, W. (2000). Bone development. Ann. Rev. Cell. Dev. Biol. 16:191–220.
  • Zhang, S.H., Reddick, R.L., Piedrahita, J.A., and Maeda, N. (1992). Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E. Science 258:468–471.
  • Plump, A.S., Smith, J.D., Hayek, T., Aalto-Setala, K., Walsh, A., Verstuyft, J.G., Rubin, E.M., and Breslow, J.L. (1992). Severe hypercholesterolemia and atherosclerosisin apolipoprotein E-deficient mice created by homol- ogous recombination in ES cells. Cell 71:343–353.
  • Schulick, A.H., Taylor, A.J., Zuo, W., Qiu, C.-B., Dong, G., Woodward, R.N., Agah, R., Roberts, A.B., Virmani, R., and Dichek, D.A. (1998). Overexpression of transforming growth factor ß1 in arterial endothelium causes hyperplasia, apoptosis, and cartilaginous metaplasia. Proc. Natl. Acad. Sci. USA 95:6983–6988.
  • Jokinen, M.P., Clarkson, T.B., and Prichard, R.W. (1985). Recent advances in molecular pathology: Animal models in atherosclerosis research. Exp. Mol. Pathol. 42:1–28.
  • Hueper, W.C. (1939). Cartilaginous foci in the hearts of white rats and of mice. Arch. Pathol. 27:466–468.
  • Hollander, C.F. (1968). Cartilaginous focus at the base of the non-coronary semilunar valve of the aorta in rats of different ages. Exp. Gerontol. 3:303–307.
  • Seemayer, T.A., Thelmo, W.L., and Morin, J. (1973). Cartilaginous trans- formation of the aortic valve. Am. J. Clin. Pathol. 60:616–620.
  • Groom, D.A., and Starke, W.R. (1990). Cartilaginous metaplasia in calcific aortic valve disease. Am. J. Clin. Pathol. 93:809–812.
  • Yagami, K., Suh, J.-Y., Enomoto-Iwamoto, M., Koyama, E., Abrams, W.R., Shapiro, I.M., Pacifici M., and Iwamoto, M. (1999). Matrix GLA protein is a developmental regulator of chondrocytes mineralization and when constitutivevly expressed, blocks endrochondral and intramembra- nous ossification in the limb. J. Cell. Biol. 147:1097–1108.
  • Scapinelli, R., and Little, K. (1970). Observations on the mechanically in- duced differentiation of cartilage from fibrous connective tissue. J. Pathol. 101:85–91.
  • Pang, S.C., and Scott, T.M. (1981). Stereological analysis of the tunica media of the aorta and renal artery during the development of hypertension in the spontaneously hypertensive rat. J. Anat. 133:513–526.
  • Wolinsky, H. (1970). Response of the rat aortic wall to hypertension: Im- portance of comparing absolute amounts of wall components. Atheroscle- rosis 11:251–255.
  • Burke, J.M., and Ross, R. (1979). Synthesis of connective tissue macro- molecules by smooth muscle. Int. Rev. Connect. Tiss. Res. 8:119–157.
  • Wolinsky, H. (1970). Response of the rat aortic wall to hypertension: Morphological and chemical studies. Circ. Res. 26:507–522.
  • O’Rourke, M.F., and Gallagher, D.E. (1996). Pulse wave analysis. J. Hy- pertension 14:S147–S157.
  • Franklin, S.S., Khan, S.A., Wong, N.D., Larson, M.G., and Levy, D. (1999). Is pulse pressure useful in predicting coronary heart disease? The Framingham Heart Study. Circulation 100:354–360.
  • Leung, D.Y.M., Glagov, S., and Mathews, M.B. (1976). Cyclic stretching stimulates synthesis of matrix components by arterial smooth muscle cells in vitro. Science 191:475–477.
  • Sumpio, B.E., Banes, A.J., Link, W.G., and Johnson, G. (1988). Enhanced collagen production by smooth muscle cells during repetitive mechanical strain. Arch. Surg. 123:1233–1236.
  • Riser, B.L., Cortes, P., Zhao, X., Bernstein, J., Dumler, F., and Narins, R.G. (1992). Intraglomerular pressure and mesangial stretching stimu- late extracellular matrix formation in the rat. J. Clin. Invest. 90:1932–1943.
  • Fischer, G.M., Swain, M.L., and Cherian, K. (1980). Pulsatile distension and vascular collagen synthesis in the rabbit. Blood Vessels 17:216–220.
  • O’Callaghan, C.J., and Williams, B. (2000). Mechanical strain-induced extracellular matrix production by human vascular smooth muscle cells. Role of TGF-ß1. Hypertension 36:319–324.
  • Miyazono, K., Kusanagi, K., and Inoue, H. (2001). Divergence and con-vergence of TGF-beta/BMP signaling. J. Cell. Physiol. 187:265–276.
  • Weston, A.D., Rosen, V., Chandraratna, R.A., and Underhill, T.M. (2000).Regulation of skeletal progenitor differentiation by the BMP and retinoid signaling pathways. J. Cell. Biol. 148:679–690.
  • Wallin, R., Cain, D., Hutson, S.M., Sane, D.C., and Loeser, R. (2000). Modulation of the binding of matrix Gla protein (MGP) to bone morphogenetic protein-2 (BMP-2). Thromb. Haemost. 84:1039–1044.
  • Bostrom, K. (2001). Insights into the mechanism of vascular calcification. Am. J. Cardiol. 88 (suppl.):20E–22E.
  • Wight, T.N. (1996). Arterial wall. In Extracellular Matrix, W.D. Comper (ed.), pp. 175–202. (Harwood Pub., Amsterdam).

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