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KMID : 0620920100420040302
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Experimental & Molecular Medicine
2010 Volume.42 No. 4 p.302 ~ p.309
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A pertussis toxin sensitive G-protein-independent pathway is involved in serum amyloid A-induced formyl peptide receptor 2-mediated CCL2 production
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Lee Ha-Young
Kim Sang-Doo
Shim Jae-Woong
Kim Hak-Jung
Yun Jean-Ho
Baek Suk-Hwan
Kim Koan-hoi
Bae Yoe-Sik
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Abstract
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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.
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KEYWORD
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atherosclerosis, chemokine CCL2, endothelial cells, FPR2 protein, human, pertussis toxin, serum amyloid A protein
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