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). 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.
Lee
Ha Young
HY
Department of Biochemistry, College of Medicine, Dong-A University, 3-1 Dongdaesindong Seogu, Busan 602-714, Republic of Korea.
Kim
Sang Doo
SD
Shim
Jae Woong
JW
Yun
Jeanho
J
Kim
Koanhoi
K
Bae
Yoe-Sik
YS
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
C111835:CCL2 protein, human; D018932:Chemokine CCL2; C469986:FPR1 protein, human; D044042:Receptors, Formyl Peptide; D000685:Serum Amyloid A Protein