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再生的内皮细胞在动脉损伤后表达胰岛素样生长因子-I免疫反应性。

Regenerating endothelial cells express insulin-like growth factor-I immunoreactivity after arterial injury.

作者信息

Hansson H A, Jennische E, Skottner A

机构信息

Department of Histology, University of Gothenburg, Sweden.

出版信息

Cell Tissue Res. 1987 Dec;250(3):499-505. doi: 10.1007/BF00218940.

DOI:10.1007/BF00218940
PMID:3690631
Abstract

In the present study the expression of insulin-like growth factor I (IGF-I; somatomedin C) immunoreactivity was examined in endothelial cells during repair after injury to the intima in the femoral artery of adult rats. Two types of injury were examined: (1) endothelial denudation induced by the use of a catheter, and (2) vessel compression by short-term ligation. In untreated rats, arterial endothelial cells showed no or, only infrequently, low IGF-I immunoreactivity in their cytoplasm. Endothelial cells at the border to the denuded area showed increased IGF-I immunoreactivity one day after injury to the intima of the femoral artery. Thrombocytes and fibrin deposits as well as vital endothelial cells, covered by clots, were immunonegative. The maximal intensity of IGF-I immunoreactivity was reached within 3 days after insult. The IGF-I immunoreactivity in the endothelial cells remained elevated for at least 4 weeks, compared to the controls. Intimal thickenings appeared within a week after injury and many cells in these thickenings showed intense IGF-I immunoreactivity as did the covering endothelial cells. Smooth muscle cells in the media were generally immunonegative during control conditions and after endothelial denudation. Spontaneously hypertensive rats (SHR) showed, similarly to their matched controls (WKY), approximately the same patterns of IGF-I immunoreactivity in their endothelial cells both under normal conditions and after injury. It is concluded that IGF-I is likely to be involved in the repair of the intima in injured arteries.

摘要

在本研究中,检测了成年大鼠股动脉内膜损伤后修复过程中内皮细胞中胰岛素样生长因子I(IGF-I;生长调节素C)免疫反应性的表达。研究了两种损伤类型:(1)使用导管诱导的内皮剥脱,以及(2)短期结扎引起的血管压迫。在未处理的大鼠中,动脉内皮细胞在其细胞质中无IGF-I免疫反应性,或仅偶尔有低免疫反应性。股动脉内膜损伤一天后,剥脱区域边界处的内皮细胞显示IGF-I免疫反应性增加。血小板和纤维蛋白沉积物以及被血栓覆盖的存活内皮细胞呈免疫阴性。IGF-I免疫反应性在损伤后3天内达到最大强度。与对照组相比,内皮细胞中的IGF-I免疫反应性至少持续升高4周。损伤后一周内出现内膜增厚,这些增厚区域的许多细胞以及覆盖的内皮细胞均显示强烈的IGF-I免疫反应性。在对照条件下和内皮剥脱后,中膜平滑肌细胞通常呈免疫阴性。自发性高血压大鼠(SHR)与其匹配的对照大鼠(WKY)相似,在正常条件下和损伤后,其内皮细胞中IGF-I免疫反应性模式大致相同。结论是IGF-I可能参与损伤动脉内膜的修复。

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