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

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.

• Authors: Lan Sun, Tiantai Zhang, Xin Yu, Wenyu Xin, Xi Lan, Dan Zhang, Chao Huang, Guahua Du
• Journal: FEBS letters (FEBS Lett) Vol. 585 Issue 17 Pg. 2727-34 (Sep 02 2011) ISSN: 1873-3468 [Electronic] England
• PMID: 21821030 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

Chemical References

• N,N-dimethylarginine
• Arginine
• Mitogen-Activated Protein Kinase 1
• Mitogen-Activated Protein Kinase 3
• p38 Mitogen-Activated Protein Kinases

Topics

• Animals
• Arginine (analogs & derivatives, pharmacology)
• Blotting, Western
• Cell Movement (drug effects)
• Cells, Cultured
• Endothelial Cells (cytology, drug effects, metabolism)
• Humans
• Male
• Mitogen-Activated Protein Kinase 1 (genetics, metabolism)
• Mitogen-Activated Protein Kinase 3 (genetics, metabolism)
• Muscle, Smooth, Vascular (cytology)
• Myocytes, Smooth Muscle (cytology, drug effects, metabolism)
• Rats
• Signal Transduction (drug effects)
• p38 Mitogen-Activated Protein Kinases (genetics, metabolism)