Okuda Y, Adrogue H J, Nakajima T, Mizutani M, Asano M, Tachi Y, Suzuki S, Yamashita K
Department of Internal Medicine, University of Tsukuba, Ibaraki, Japan.
Life Sci. 1996;59(17):1455-61. doi: 10.1016/0024-3205(96)00473-0.
The mechanisms responsible for the abnormalities in the vascular wall associated with long standing diabetes mellitus are incompletely understood. The aim of this investigation was to assess the effects of angiotensin II and high glucose on the production of platelet-derived growth factor (PDGF) in human endothelial cells. For this purpose, a primary culture was obtained from fresh human umbilical cords by collagenase digestion of the vein interior. A high glucose medium increased the production of PDGF and a similar effect was observed by the addition of mannitol. These data are consistent with a stimulatory effect of glucose on PDGF that is mediated by the osmotic effect of this substance. Angiotensin II significantly increased PDGF in human endothelial cells and the effect was accompanied by a transient increase in cytosolic calcium. The angiotensin II-induced intracellular Ca2+ increases, PDGF production were completely abolished by saralasin and neomycin, respectively. We postulate that the increased production of PDGF by the vascular endothelium in response to high glucose and angiotensin II may participate in the development of the diabetic angiopathy.
与长期糖尿病相关的血管壁异常的发病机制尚未完全明确。本研究旨在评估血管紧张素II和高糖对人内皮细胞中血小板衍生生长因子（PDGF）产生的影响。为此，通过对新鲜人脐带静脉内部进行胶原酶消化获得原代培养物。高糖培养基增加了PDGF的产生，添加甘露醇也观察到类似效果。这些数据与葡萄糖通过该物质的渗透作用对PDGF产生刺激作用一致。血管紧张素II显著增加人内皮细胞中的PDGF，且该作用伴随着胞质钙的短暂增加。血管紧张素II诱导的细胞内Ca2+增加和PDGF产生分别被沙拉新和新霉素完全消除。我们推测，血管内皮细胞对高糖和血管紧张素II反应导致的PDGF产生增加可能参与糖尿病血管病变的发展。
