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CCL2 — SAA1

Text-mined interactions from Literome

Lee et al., J Immunol 2008 : In the present study, we investigated the effect of SAA on the production of CCL2 , an important mediator of monocyte recruitment, and the mechanism underlying the action of SAA in human monocytes ... Moreover, SAA induced CCL2 induction was inhibited by a formyl peptide receptor-like 1 (FPRL1) antagonist ... Taken together, our findings suggest that SAA stimulates CCL2 production and, thus, contributes to atherosclerosis ... Moreover, FPRL1 was found to be engaged in SAA induced CCL2 induction, and cyclooxygenase-2 induction was found to be essential for SAA induced CCL2 expression
Lee et al., Biochem Biophys Res Commun 2009 (Atherosclerosis) : Activation of formyl peptide receptor like-1 by serum amyloid A induces CCL2 production in human umbilical vein endothelial cells ... We investigated the effects of serum amyloid A (SAA) on the production of C-C chemokine motif ligand 2 (CCL2) and the mechanism underlying SAA action in human umbilical vein endothelial cells ( HUVECs ) ... HUVECs expressed formyl peptide receptor-like 1 (FPRL1), and short interfering RNA knockdown of FPRL1 nearly completely blocked SAA induced CCL2 production in HUVECs ... We suggest that SAA stimulates CCL2 production via FPRL1 and, thus, contributes to atherosclerosis
Lee et al., Exp Mol Med 2010 : Serum amyloid A (SAA) induced CCL2 production via a pertussis toxin ( PTX ) -insensitive pathway in human umbilical vein endothelial cells ( HUVECs ) ... 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 ... 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
Li et al., Oncogene 2011 (Neoplasms) : Here, we showed that serum amyloid-A (SAA) and cathelicidin ( LL-37 ) stimulated M-CSF and MCP-1 expression with or without lipopolysaccharide (LPS) administration ; conversely, lipoxin-A ( 4 ) ( LXA ( 4 ) ) and annexin-A1 (ANXA1) inhibited LPS induced M-CSF and MCP-1 production by human ( HepG2 ) and mouse ( H22 ) hepatocellular carcinoma cells (HCCs)