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

Lan Sun, Tiantai Zhang, Xin Yu, Wenyu Xin, Xi Lan, Dan Zhang, Chao Huang, Guahua Du

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish (US)
Pages (from-to)2727-2734
Number of pages8
JournalFEBS Letters
Volume585
Issue number17
DOIs
StatePublished - Sep 2 2011
Externally publishedYes

Keywords

  • Asymmetric dimethylarginine
  • Atherosclerosis
  • MAPK
  • Migration
  • Oxide LDL
  • Vascular smooth muscle cell

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

Fingerprint Dive into the research topics of 'Asymmetric dimethylarginine confers the communication between endothelial and smooth muscle cells and leads to VSMC migration through p38 and ERK1/2 signaling cascade'. Together they form a unique fingerprint.

Cite this