Hahn A W, Kern F, Jonas U, John M, Bühler F R, Resink T J
Department of Research, University Clinics Basel, Switzerland.
J Vasc Res. 1995 May-Jun;32(3):162-74. doi: 10.1159/000159090.
The arterial tenascin C expression in vivo and in vitro has been studied using immunohistochemistry. The functional relevance of localized tenascin C expression was assessed in vitro using various human cell types involved in the progression of vascular disease. Normotensive and hypertensive rats exhibited age-dependent patterns of vascular (aorta) tenascin expression, but the lumen-to-media-directed progression of tenascin induction was accelerated in hypertensive rats. Tenascin-rich neointimal lesions (spontaneous) were observed at branching sites of aorta from aged (80 weeks) hypertensive rats. Subendothelial tenascin foci contained lipid-laden smooth muscle cells and monocytes/macrophages. Medial tenascin foci encaged smooth muscle cells which synthesized DNA. Tenascin was expressed both in vivo and in vitro by endothelial and smooth muscle cells but not by monocytes/macrophages; angiotensin II, oxidized-low density lipoprotein and transforming growth factor beta 1 induced expression of tenascin transcripts and glycoprotein in vitro. Endothelial and smooth muscle cells, but not monocytes, adhered to tenascin substrata. Tenascin reduced focal adhesion integrity in confluent endothelial and smooth muscle cell cultures. Angiotensin II-induced migration of endothelial and smooth muscle cells was accompanied by tenascin deposition within extracellular matrix migration trails. Tenascin may function both as a defense against monocyte invasion and medial smooth muscle replication, as well as a substratum for directed endothelial and smooth muscle cell migration.
已使用免疫组织化学方法研究了体内和体外动脉腱生蛋白C的表达。使用参与血管疾病进展的各种人类细胞类型在体外评估了局部腱生蛋白C表达的功能相关性。正常血压和高血压大鼠表现出血管（主动脉）腱生蛋白表达的年龄依赖性模式，但腱生蛋白诱导的从管腔到中膜的进展在高血压大鼠中加速。在老年（80周）高血压大鼠主动脉的分支部位观察到富含腱生蛋白的新生内膜病变（自发的）。内皮下腱生蛋白病灶含有载脂平滑肌细胞和单核细胞/巨噬细胞。中膜腱生蛋白病灶包裹着合成DNA的平滑肌细胞。内皮细胞和平滑肌细胞在体内和体外均表达腱生蛋白，而单核细胞/巨噬细胞不表达；血管紧张素II、氧化型低密度脂蛋白和转化生长因子β1在体外诱导腱生蛋白转录本和糖蛋白的表达。内皮细胞和平滑肌细胞而非单核细胞黏附于腱生蛋白基质。腱生蛋白降低了汇合的内皮细胞和平滑肌细胞培养物中的黏着斑完整性。血管紧张素II诱导的内皮细胞和平滑肌细胞迁移伴随着细胞外基质迁移轨迹内腱生蛋白的沉积。腱生蛋白可能既作为抵御单核细胞侵袭和中膜平滑肌复制的防御物质，又作为内皮细胞和平滑肌细胞定向迁移的基质。
