Mackie E J, Scott-Burden T, Hahn A W, Kern F, Bernhardt J, Regenass S, Weller A, Bühler F R
Department of Research, Basel University Hospital, Switzerland.
Am J Pathol. 1992 Aug;141(2):377-88.
The extracellular matrix glycoprotein tenascin is associated with remodeling events in many embryonic and pathologic tissues. The expression of tenascin has been investigated by immunohistochemistry in blood vessels of Wistar-Kyoto (normotensive) and spontaneously hypertensive rats. Weak tenascin staining was present throughout the tunica media of large and small arteries from normotensive animals; strong staining was only detectable at branching sites. In arteries from hypertensive animals, foci of strong tenascin staining were scattered throughout the tunica media. The expression of tenascin mRNA and protein by rat aortic smooth muscle cells cultured in serum-free medium was induced by the vasoconstrictor peptide angiotensin II. Transforming growth factor-beta and platelet-derived growth factor also stimulated tenascin mRNA expression. Vascular smooth muscle cells attached specifically to a substratum of tenascin, but remained rounded. Thus, increased focal tenascin expression by vascular smooth muscle cells is associated with hypertension, and may mediate angiotensin II-induced changes in vascular structure in hypertension.
细胞外基质糖蛋白腱生蛋白与许多胚胎组织和病理组织中的重塑事件相关。已通过免疫组织化学方法研究了Wistar - Kyoto（正常血压）大鼠和自发性高血压大鼠血管中腱生蛋白的表达。正常血压动物的大动脉和小动脉中膜全程均有弱的腱生蛋白染色；仅在分支部位可检测到强染色。在高血压动物的动脉中，强腱生蛋白染色灶散在分布于整个中膜。在无血清培养基中培养的大鼠主动脉平滑肌细胞中，血管收缩肽血管紧张素II可诱导腱生蛋白mRNA和蛋白的表达。转化生长因子-β和血小板衍生生长因子也刺激腱生蛋白mRNA表达。血管平滑肌细胞特异性附着于腱生蛋白基质，但仍保持圆形。因此，血管平滑肌细胞局灶性腱生蛋白表达增加与高血压相关，且可能介导高血压中血管紧张素II诱导的血管结构变化。
