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Asymmetric dimethylarginine confers the communication between endothelial and smooth muscle cells and leads to VSMC migration through p38 and ERK1/2 signaling cascade
Author(s) -
Sun Lan,
Zhang Tiantai,
Yu Xin,
Xin Wenyu,
Lan Xi,
Zhang Dan,
Huang Chao,
Du Guahua
Publication year - 2011
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2011.07.032
Subject(s) - asymmetric dimethylarginine , vascular smooth muscle , microbiology and biotechnology , signal transduction , smooth muscle , endothelial dysfunction , medicine , mapk/erk pathway , endocrinology , chemistry , biology , arginine , biochemistry , amino acid
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.