不对称二甲基精氨酸通过 p38 和 ERK1/2 信号级联赋予内皮细胞和平滑肌细胞之间的通讯，并导致 VSMC 迁移。

Asymmetric dimethylarginine confers the communication between endothelial and smooth muscle cells and leads to VSMC migration through p38 and ERK1/2 signaling cascade.

机构信息

National Center for Pharmaceutical Screening, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.

出版信息

FEBS Lett. 2011 Sep 2;585(17):2727-34. doi: 10.1016/j.febslet.2011.07.032. Epub 2011 Aug 2.

DOI:10.1016/j.febslet.2011.07.032

PMID:21821030

Abstract

Communication between endothelial and smooth muscle cells (SMCs) contributes to atherosclerosis induced by atherogenic factors, such as oxide LDL. Asymmetric dimethylarginine (ADMA), a newly found cardiovascular risk factor, accumulates in the culture medium of oxide LDL (oxLDL)-treated endothelial cells and positively correlates with atherosclerosis. This study demonstrates that ADMA mediates the communication between endothelial cells and SMCs induced by oxLDL leading to SMC migration. In addition, the present study suggests exogenous ADMA directly induces SMC migration via p38 and ERK1/2 MAPK signaling transduction way. Investigations to identify the factors regulating VSMC migration may provide novel insights into atherosclerosis and its complications.

摘要

内皮细胞和平滑肌细胞（SMCs）之间的通讯有助于动脉粥样硬化的形成，这种形成是由动脉粥样硬化因子引起的，如氧化型 LDL。不对称二甲基精氨酸（ADMA）是一种新发现的心血管危险因素，它在内皮细胞经氧化型 LDL（oxLDL）处理后的培养液中积累，并与动脉粥样硬化呈正相关。本研究表明 ADMA 介导 oxLDL 诱导的内皮细胞和 SMC 之间的通讯，导致 SMC 迁移。此外，本研究表明外源性 ADMA 通过 p38 和 ERK1/2 MAPK 信号转导途径直接诱导 SMC 迁移。对调节 VSMC 迁移的因素的研究可能为动脉粥样硬化及其并发症提供新的见解。