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亲环素A是一种由氧化应激诱导产生的分泌型生长因子。

Cyclophilin A is a secreted growth factor induced by oxidative stress.

作者信息

Jin Z G, Melaragno M G, Liao D F, Yan C, Haendeler J, Suh Y A, Lambeth J D, Berk B C

机构信息

Center for Cardiovascular Research, University of Rochester, Rochester, NY, USA.

出版信息

Circ Res. 2000 Oct 27;87(9):789-96. doi: 10.1161/01.res.87.9.789.

Abstract

Reactive oxygen species have been implicated in the pathogenesis of atherosclerosis, hypertension, and restenosis, in part by promoting vascular smooth muscle cell (VSMC) growth. Many VSMC growth factors are secreted by VSMC and act in an autocrine manner. Here we demonstrate that cyclophilin A (CyPA), a member of the immunophilin family, is secreted by VSMCs in response to oxidative stress and mediates extracellular signal-regulated kinase (ERK1/2) activation and VSMC growth by reactive oxygen species. Human recombinant CyPA can mimic the effects of secreted CyPA to stimulate ERK1/2 and cell growth. The peptidyl-prolyl isomerase activity is required for ERK1/2 activation by CyPA. In vivo, CyPA expression and secretion are increased by oxidative stress and vascular injury. These findings are the first to identify CyPA as a secreted redox-sensitive mediator, establish CyPA as a VSMC growth factor, and suggest an important role for CyPA and enzymes with peptidyl-prolyl isomerase activity in the pathogenesis of vascular diseases.

摘要

活性氧已被认为参与动脉粥样硬化、高血压和再狭窄的发病机制,部分原因是其促进血管平滑肌细胞(VSMC)生长。许多VSMC生长因子由VSMC分泌并以自分泌方式起作用。在此我们证明,亲环素A(CyPA)作为亲免素家族的一员,由VSMC在氧化应激反应中分泌,并通过活性氧介导细胞外信号调节激酶(ERK1/2)的激活和VSMC生长。人重组CyPA可模拟分泌型CyPA的作用,刺激ERK1/2和细胞生长。CyPA激活ERK1/2需要肽基脯氨酰异构酶活性。在体内,氧化应激和血管损伤会增加CyPA的表达和分泌。这些发现首次将CyPA鉴定为一种分泌型氧化还原敏感介质,确立了CyPA作为一种VSMC生长因子,并提示CyPA和具有肽基脯氨酰异构酶活性的酶在血管疾病发病机制中具有重要作用。

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