A pertussis toxin sensitive G-protein-independent pathway is involved in serum amyloid A-induced formyl peptide receptor 2-mediated CCL2 production

作者：Lee Ha Young; Kim Sang Doo; Shim Jae Woong; Kim Hak Jung; Yun Jeanho; Baek Suk Hwan; Kim Koanhoi; Bae Yoe Sik^*

来源：Experimental and Molecular Medicine, 2010, 42(4): 302-309.

DOI：10.3858/emm.2010.42.4.029

• atherosclerosis
• chemokine CCL2
• endothelial cells
• FPR2 protein, human
• pertussis toxin
• serum amyloid A protein

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 G, 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.

• 出版日期2010-4-30