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肝素衍生寡糖对血管平滑肌细胞增殖的影响。

Effect of heparin-derived oligosaccharide on vascular smooth muscle cell proliferation.

作者信息

Li Li, Li Wei, Ren Zhong, He ShuYing, Xu GuangLin, Yang LiNa

机构信息

School of Life Science and Technology, China Pharmaceutical University, Nanjing, China.

出版信息

Vasc Endovascular Surg. 2012 Jul;46(5):393-400. doi: 10.1177/1538574412442595. Epub 2012 May 17.

Abstract

In this study, the effect of heparin-derived oligosaccharide on bovine vascular smooth muscle cell (VSMC) proliferation and signal transduction mechanism was investigated. Extracellular-signal-regulated kinase (ERK) 1/2 has been implicated in the regulation of various cellular functions including proliferation, and we sought to define a functional role for ERK 1/2 in an established proliferation model in order to find a possible mechanism for inhibition of VSMC proliferation by heparin-derived oligosaccharide. The VSMC proliferation model was developed by platelet-derived growth factor (PDGF), and the level of ERK 1/2 protein and messenger RNA was determined by reverse transcriptase-polymerase chain reaction, Western blotting, and immunocytochemical methods. Flow cytometry analysis indicated that heparin-derived oligosaccharide blocked PDGF-induced cell cycle progression by arresting cells in the G0/G1 phase. The results imply that heparin-derived oligosaccharide inhibits VSMC proliferation by moderating the gene and the phosphorylation levels of ERK 1/2, eventually blocking G1/S transition, may be one of the mechanisms for inhibition of VSMC proliferation by heparin-derived oligosaccharide.

摘要

本研究探讨了肝素衍生寡糖对牛血管平滑肌细胞(VSMC)增殖及信号转导机制的影响。细胞外信号调节激酶(ERK)1/2参与包括增殖在内的多种细胞功能的调节,我们试图在已建立的增殖模型中确定ERK 1/2的功能作用,以便找到肝素衍生寡糖抑制VSMC增殖的可能机制。VSMC增殖模型由血小板衍生生长因子(PDGF)构建,通过逆转录-聚合酶链反应、蛋白质印迹法和免疫细胞化学方法测定ERK 1/2蛋白和信使RNA的水平。流式细胞术分析表明,肝素衍生寡糖通过使细胞停滞在G0/G1期来阻断PDGF诱导的细胞周期进程。结果表明,肝素衍生寡糖可能通过调节ERK 1/2的基因和磷酸化水平来抑制VSMC增殖,最终阻断G1/S期转换,这可能是肝素衍生寡糖抑制VSMC增殖的机制之一。

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