Summary
The tenascins are a family of extracellular matrix proteins. Tenascin-C (TNC) is expressed during embryogenesis or cancer invasion. Tenascin-X (TNX) is ubiquitously expressed, with the highest levels in the heart. To clarify the role of TNC and TNX in the heart, we analyzed TNC and TNX expression patterns in embryonic hearts of mice by immunohistochemistry and in situ hybridization. TNC was transiendy expressed at four important steps of early heart development: (1) differentiation of cardiomyocytes from the mesoderm, (2) formation of endocardial cushion tissue, (3) development of the outflow tract, and (4) migration of the proepicardial cells (precursors of coronary vessels). After the expression of TNC was downregulated, TNX was expressed by epicardial cells invading the myocardial layer and forming vascular channels. In normal adult hearts, TNC was sparse but reappeared under pathological conditions. During tissue repair after electric injury to the ventricle of mice, TNC appeared at the border zone between intact and injured myocardium, the most active sites of tissue remodeling during the acute stage. These expression patterns strongly suggest the important roles of TNC in tissue remodeling of the myocardium as well as during early heart development. However, in TNC knockout mice, the heart developed normally, and the myocardial tissue repair seemed to proceed normally. Furthermore, our findings did not show that TNX compensates for the loss of TNC.
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References
Chiquet-Ehrismann R, Mackie EJ, Pearson CA, Sakakura T. 1986.Tenascin interferes with fibronectin action. Cell 53:383–390.
Prieto AL, Anderson-Fisone C, Crossin KL. 1992. Characterization of multiple adhesive and coun-teradhesive domains in the extracellular matrix protein cytotactin.J Cell Biol 119:663–678.
Matsumoto K, Saga Y, Ikemura T, Sakakura T, Chiquet-Ehrismann R. 1994. The distribution of tenascin-X is distinct and often reciprocal to that of tenascin-C. J Cell Biol 125:483–493.
Tamura A, Kusachi S, Nogami K, Yamanishi A, Kajikawa Y, Hirohata S, Tsuji T. 1996.Tenascin expression in endomyocardial biopsy specimens in patients with dilated cardiomyopathy: distribution along margins of fibrotic lesions. Heart 75:291–294.
Willems IE, Arends JW, Daemen MJ. 1996. Tenascin and fibronectin expression in healing human myocardial scars. J Pathol 179:321–325.
Hasegawa K, Yoshida T, Matsumoto K, Katsuta K, Waga S, Sakakura T. 1997. Differential expression of tenascin-C and tenascin-X in human astrocytomas. Acta Neuropathol 93:431–437.
Kataoka H, Takakura N, Nishikawa S, Tsuchida K, Kodama H, Kunisada T, Risau W, Kita T, Nishikawa SI. 1997. Expressions of PDGF receptor alpha, c-Kit and Flkl genes clustering in mouse chromosome 5 define distinct subsets of nascent mesodermal cells. Dev Growth Differ 39:729–740.
Kalembey I, Yoshida T, Iriyama K, Sakakura T. 1997. Analysis of tenascin mRNA expression in the murine mammary gland from embryogenesis to carcinogenesis: an in situ hybridization study. Int J Dev Biol 41:569–573.
Ishihara A, Yoshida T.Tamaki H, Sakakura T. 1995. Tenascin expression in cancer cells and stroma of human breast cancer and its prognostic significance. Clin Cancer Res 1:1035–1041.
Markwald RR, Fitzharris TP, Smith A. 1975. Structural analysis of endocardial cytodifferentiation. Dev Biol 42:160–180.
Markwald RR, Fitzharris TP, Manasck FJ. 1977. Structural development of endocardial cushions. Am J Anat 148:85–119.
Komiyama M, Ito K, Shimada Y. 1987. Origin and development of the epicardium in the mouse embryo. Anat Embryol 176:183–189.
Poelmann RE, Gittenberger-de Groot AC, Mentink MMT, Bokenkamp R, Hogers B. 1993. Development of the cardiac coronary vascular endothelium, studied with antiendothelial antibodies in chicken quail chimeras. Circ Res 73:559–568.
Mikawa T, Fischman DA. 1992. Retroviral analysis of cardiac morphogenesis: discontinuous formation of cardiac vessels. Proc Natl Acad Sci USA 89:9504–9508.
Imanaka-Yoshida K, Ishiyama S, Shimojo T, Hiroe M, Ohta T, Nishikawa T, Yoshida T, Sakakura T 1997. A possible role of tenascin-C in tissue remodeling after myocardial infarction. J Mol Cell Cardiol 29:A291.
Imanaka-Yoshida K, Danowski BA, Sanger JM, Sanger JW. 1994.Vinculin-containing costameres: part of contraction force transmission sites of cardiomyocytes. In The Cardiomyopathic Heart. Ed. M. Nagano, N. Takeda, and N.S. Dalla, 245–255. New York: Raven Press.
Imanaka-Yoshida K, Danowski BA, Sanger JM, Sanger JW. 1996. Living adult rat cardiomyocytes in culture: evidence for dissociation of castameric distribution of vinculin from costameric distributions of attachments. Cell Motil Cytoskel 33:263–275.
Imanaka-Yoshida K, Enomoto-Iwamoto M, Yoshida T, Sakakura T. 1999.Vinculin, talin, integrin α6β1 and laminin can serve as components of attachment complex mediating contraction force transmission from cardiomyocytes to extracellular matrix. Cell Motil Cytoskel 42:1–11.
Danowski BA, Imanaka-Yoshida K, Sanger JM, Sanger JW. 1992. Costameres are sites of force transmission to the substratum in adult rat cardiomyocytes. J Cell Biol 118:1411–1420.
Imanaka-Yoshida K, Sanger JM, Sanger JW. 1993. Contractile protein dynamics of myofibrils in paired adult rat cardiomyocytes. Cell Motil Cytoskel 26:301–312.
Vracko R, Thorning D, Frederickson RG, Cunningham D. 1988. Myocyte reactions at the borders of injured and healing rat myocardium. Lab Invest 59:104–114.
Saga YYagi T, Ikawa Y, Sakakura T, Aizawa S. 1992. Mice develop normally without tenascin. Genes Dev 6:1821–1831.
Forsberg E, Hirsh E, Frohlich L, Meyer M, Ekblom M, Aszodi A, Werner S, Fassler R. 1996. Skin wounds and nerves heal normally in mice lacking tenascin-C. Proc Natl Acad Sci USA 93:6594–6599.
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Imanaka-Yoshida, K., Yokoyama, K., Sakakura, T. (2000). Possible Roles of the Tenascin Family During Heart Development and Myocardial Tissue Remodeling. In: Takeda, N., Nagano, M., Dhalla, N.S. (eds) The Hypertrophied Heart. Progress in Experimental Cardiology, vol 3. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4423-4_10
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DOI: https://doi.org/10.1007/978-1-4615-4423-4_10
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