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Sphingosine 1‐phosphate (S1P) inhibits monocyte–endothelial cell interaction by regulating of RhoA activity
Author(s) -
Tani Mariko,
Kawakami Akio,
Nagai Miyuzu,
Shimokado Kentaro,
Kondo Kazuo,
Yoshida Masayuki
Publication year - 2007
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.2007.08.053
Subject(s) - rhoa , sphingosine 1 phosphate , sphingosine , umbilical vein , microbiology and biotechnology , monocyte , chemistry , endothelial stem cell , phorbol , cell adhesion , signal transduction , biochemistry , cell , protein kinase c , biology , receptor , in vitro , immunology
Recent studies suggest that sphingosine 1‐phosphate (S1P) protects against atherosclerosis. We assessed the effects of S1P on monocyte–endothelial interaction in the presence of inflammatory mediators. Pretreatment of THP‐1 cells with S1P abolished Phorbol 12 myristate 13‐acetate (PMA)‐induced THP‐1 cell adhesion to human umbilical vein endothelial cells (HUVECs). S1P inhibited PMA‐induced activation of RhoA, but not PKCs. S1P activated p190Rho GTPase activation protein (GAP) only in the presence of PMA, suggesting an inhibitory effect of S1P and PMA to suppress RhoA. In conclusion, S1P inhibited monocyte–endothelial interactions by inhibiting RhoA activity which may explain its anti‐atherogenic effects.