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动脉平滑肌细胞在内皮损伤时会表达一氧化氮合酶。

Arterial smooth muscle cells express nitric oxide synthase in response to endothelial injury.

作者信息

Hansson G K, Geng Y J, Holm J, Hårdhammar P, Wennmalm A, Jennische E

机构信息

Department of Clinical Chemistry, Gothenburg University, Sweden.

出版信息

J Exp Med. 1994 Aug 1;180(2):733-8. doi: 10.1084/jem.180.2.733.

DOI:10.1084/jem.180.2.733
PMID:7519246
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2191619/
Abstract

Endothelial cells regulate vascular tone by secreting paracrine mediators that control the contractility of arterial smooth muscle cells. Nitric oxide (NO) is an important vasodilating agent that is generated from L-arginine by the enzyme nitric oxide synthase (NOS), which is expressed constitutively by the endothelium. NO also inhibits platelet aggregation, contributing to the antithrombotic properties of the endothelial surface. It would therefore be expected that loss of the endothelium during arterial injury would lead to vasospasm and thrombosis but instead, the neointima formed after injury has a nonthrombogenic surface and a maintained vascular patency. We report here that arterial smooth muscle cells in the neointima formed after a deendothelializing balloon injury to the rat carotid artery express the cytokine-inducible isoform of NOS. Expression was detectable by reverse transcription-polymerase chain reaction from day 1-14 after injury and in situ hybridization showed expression of NOS mRNA by neointimal smooth muscle cells, particularly at the surface of the lesion. This was associated with systemically detectable NO production as revealed by electron paramagnetic resonance spectroscopic analysis of nitrosylated red cell hemoglobin. Local NO production by intimal smooth muscle cells after endothelial injury could represent an important mechanism for the maintenance of arterial patency and nonthrombogenicity in the injured artery.

摘要

内皮细胞通过分泌旁分泌介质来调节血管张力,这些介质控制动脉平滑肌细胞的收缩性。一氧化氮(NO)是一种重要的血管舒张剂,由一氧化氮合酶(NOS)催化L-精氨酸生成,内皮细胞组成性表达该酶。NO还抑制血小板聚集,有助于内皮表面的抗血栓特性。因此可以预期,动脉损伤期间内皮细胞丧失会导致血管痉挛和血栓形成,但相反,损伤后形成的新生内膜具有非血栓形成表面且血管通畅得以维持。我们在此报告,大鼠颈动脉去内皮球囊损伤后形成的新生内膜中的动脉平滑肌细胞表达细胞因子诱导型NOS同工型。损伤后第1至14天通过逆转录-聚合酶链反应可检测到表达,原位杂交显示新生内膜平滑肌细胞表达NOS mRNA,尤其是在病变表面。如通过亚硝基化红细胞血红蛋白的电子顺磁共振光谱分析所揭示,这与全身可检测到的NO生成相关。内皮损伤后内膜平滑肌细胞局部产生NO可能是损伤动脉维持血管通畅和非血栓形成的重要机制。

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