A pertussis toxin sensitive G-protein-independent pathway is involved in serum amyloid A-induced formyl peptide receptor 2-mediated CCL2 production.
10.3858/emm.2010.42.4.029
- Author:
Ha Young LEE
1
;
Sang Doo KIM
;
Jae Woong SHIM
;
Hak Jung KIM
;
Jeanho YUN
;
Suk Hwan BAEK
;
Koanhoi KIM
;
Yoe Sik BAE
Author Information
1. Department of Biological Science, Sungkyunkwan University, Suwon 440-746, Korea. yoesik@skku.edu
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
atherosclerosis;
chemokine CCL2;
endothelial cells;
FPR2 protein, human;
pertussis toxin;
serum amyloid A protein
- From:Experimental & Molecular Medicine
2010;42(4):302-309
- CountryRepublic of Korea
- Language:English
-
Abstract:
Serum amyloid A (SAA) induced CCL2 production via a pertussis toxin (PTX)-insensitive pathway in human umbilical vein endothelial cells (HUVECs). SAA induced the activation of three MAPKs (ERK, p38 MAPK, and JNK), which were completely inhibited by knock-down of formyl peptide receptor 2 (FPR2). Inhibition of p38 MAPK and JNK by their specific inhibitors (SB203580 and SP600125), or inhibition by a dominant negative mutant of p38 MAPK dramatically decreased SAA-induced CCL2 production. Inactivation of Gi protein(s) by PTX inhibited the activation of SAA-induced ERK, but not p38 MAPK or JNK. The results indicate that SAA stimulates FPR2-mediated activation of p38 MAPK and JNK, which are independent of a PTX-sensitive G-protein and are essential for SAA-induced CCL2 production.
