Hahn A W, Kern F, Bühler F R, Resink T J
Departement Innere Medizin, Kantonsspital Basel.
Clin Investig. 1993;71(5 Suppl):S7-12. doi: 10.1007/BF00180070.
A hallmark of vascular disease is the inappropriate proliferative and synthetic behaviour of vascular smooth muscle cells. This phenotypically immature behaviour arises as a consequence of the myocytes undergoing phenotypic conversion and/or clonal proliferation of a "fetal" type of smooth muscle cell preexisting in the vessel wall. De-differentiation and initiation of proliferation is not only induced by endothelial desquamation and acute exposure of smooth muscle cells to platelet-derived mitogens, but also occurs in the uninjured blood vessel. Therefore normal components of the blood vessel are implicit in the pathological process. These include vasoconstrictor peptides, growth factor peptides and extracellular matrix molecules. In vitro and in vivo experimentation has indicated that while some of these compounds individually are only mild stimulators of smooth muscle proliferative metabolism, they may act synergistically to induce robust responses. Here we discuss the effects of the vasoconstrictor peptide angiotensin II, which can be locally generated within the vessel wall itself, on the expression of extracellular matrix molecules in vitro and in vivo. We focus on the angiotensin II-modulated expression of extracellular matrix glycoproteins, e.g. thrombospondin, tenascin, fibronectin and laminin.
血管疾病的一个标志是血管平滑肌细胞出现不适当的增殖和合成行为。这种表型不成熟的行为是由于肌细胞经历表型转化和/或血管壁中预先存在的“胎儿”型平滑肌细胞的克隆增殖所致。去分化和增殖的启动不仅由内皮剥脱和平滑肌细胞急性暴露于血小板衍生的有丝分裂原诱导，也发生在未受损的血管中。因此，血管的正常成分在病理过程中起着重要作用。这些成分包括血管收缩肽、生长因子肽和细胞外基质分子。体外和体内实验表明，虽然这些化合物中的一些单独作用时只是平滑肌增殖代谢的轻度刺激剂，但它们可能协同作用以诱导强烈反应。在这里，我们讨论血管收缩肽血管紧张素II（可在血管壁自身局部产生）对体外和体内细胞外基质分子表达的影响。我们重点关注血管紧张素II调节的细胞外基质糖蛋白的表达，例如血小板反应蛋白、腱生蛋白、纤连蛋白和层粘连蛋白。
