title: Activation of formyl peptide receptor like-1 by serum amyloid A induces CCL2 production in human umbilical vein endothelial cells.
abstract: 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). Stimulation of HUVECs by SAA elicited CCL2 production in a concentration-dependent manner. SAA induced the activations of NF-kappaB and AP-1, which were essential for CCL2 production after SAA stimulation. 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.
authors.affiliation: Department of Biochemistry, College of Medicine, Dong-A University, 3-1 Dongdaesindong Seogu, Busan 602-714, Republic of Korea.
authors.forename: Ha Young
authors.initials: HY
authors.lastname: Lee
authors.forename: Sang Doo
authors.initials: SD
authors.lastname: Kim
authors.forename: Jae Woong
authors.initials: JW
authors.lastname: Shim
authors.forename: Jeanho
authors.initials: J
authors.lastname: Yun
authors.forename: Koanhoi
authors.initials: K
authors.lastname: Kim
authors.forename: Yoe-Sik
authors.initials: YS
authors.lastname: Bae
mesh_terms: D050197:Atherosclerosis / Q000378:metabolism*; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000096:biosynthesis*; D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D044042:Receptors, Formyl Peptide / Q000819:agonists* / Q000235:genetics / Q000378:metabolism; D000685:Serum Amyloid A Protein / Q000378:metabolism* / Q000494:pharmacology; D014471:Umbilical Veins / Q000166:cytology / Q000187:drug effects / Q000378:metabolism
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; C469986:FPR1 protein, human; D044042:Receptors, Formyl Peptide; D000685:Serum Amyloid A Protein