Activation of formyl peptide receptor like-1 by serum amyloid A induces CCL2 production in human umbilical vein endothelial cells

被引：25

作者：

Lee, Ha Young ^{[1
]}

Kim, Sang Doo ^{[1
]}

Shim, Jae Woong ^{[1
]}

Yun, Jeanho ^{[1
]}

Kim, Koanhoi ^{[2
]}

Bae, Yoe-Sik ^{[1
]}

机构：

[1] Dong A Univ, Coll Med, Dept Biochem, Pusan 602714, South Korea

[2] Pusan Natl Univ, Coll Med, Dept Pharmacol, Pusan 602739, South Korea

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2009年 / 380卷 / 02期

关键词：

Serum amyloid A; C-C chemokine motif ligand 2; Formyl peptide receptor like-1; Endothelial cells; Atherosclerosis; ACUTE-PHASE REACTANT; MONOCYTE CHEMOATTRACTANT; HUMAN NEUTROPHILS; APOLIPOPROTEIN-E; KAPPA-B; A SAA; ATHEROSCLEROSIS; PROTEIN; MICE; BINDING;

D O I：

10.1016/j.bbrc.2009.01.068

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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-kappa B 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. (c) 2009 Elsevier Inc. All rights reserved.

引用

页码：313 / 317

页数：5

共 31 条

[1] SERUM AMYLOID-A IS A CHEMOATTRACTANT - INDUCTION OF MIGRATION, ADHESION, AND TISSUE INFILTRATION OF MONOCYTES AND POLYMORPHONUCLEAR LEUKOCYTES
BADOLATO, R
WANG, JM
MURPHY, WJ
LLOYD, AR
MICHIEL, DF
BAUSSERMAN, LL
KELVIN, DJ
OPPENHEIM, JJ
[J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1994, 180 (01) : 203 - 209
[2] Serum amyloid a binding to CLA-1 (CD36 and LIMPII analogous-1) mediates serum amyloid A protein-induced activation of ERK1/2 and p38 mitogen-activated protein kinases
Baranova, IN
Vishnyakova, TG
Bocharov, AV
Kurlander, R
Chen, ZG
Kimelman, ML
Remaley, AT
Csako, G
Thomas, F
Eggerman, TL
Patterson, AP
[J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (09) : 8031 - 8040
[3] Decreased lesion formation in CCR2-/- mice reveals a role for chemokines in the initiation of atherosclerosis
Boring, L
Gosling, J
Cleary, M
Charo, IF
[J]. NATURE, 1998, 394 (6696) : 894 - 897
[4] Serum amyloid A is a ligand for scavenger receptor class B type I and inhibits high density lipoprotein binding and selective lipid uptake
Cai, L
de Beer, MC
de Beer, FC
van der Westhuyzen, DR
[J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (04) : 2954 - 2961
[5] Serum amyloid A inhibits apoptosis of human neutrophils via a P2X7-sensitive pathway independent of formyl peptide receptor-like 1
Christenson, Karin
Bjoerkman, Lena
Taengemo, Carolina
Bylund, Johan
[J]. JOURNAL OF LEUKOCYTE BIOLOGY, 2008, 83 (01) : 139 - 148
[6] Microcirculation and oxidative stress
Crimi, E.
Ignarro, L. J.
Napoli, C.
[J]. FREE RADICAL RESEARCH, 2007, 41 (12) : 1364 - 1375
[7] Davenpeck KL, 1998, J IMMUNOL, V161, P6861
[8] Angiotensin IV activates the nuclear transcription factor-κB and related proinflammatory genes in vascular smooth muscle cells
Esteban, V
Ruperez, M
Sánchez-López, E
Rodríguez-Vita, J
Lorenzo, O
Demaegdt, H
Vanderheyden, P
Egido, J
Ruiz-Ortega, MR
[J]. CIRCULATION RESEARCH, 2005, 96 (09) : 965 - 973
[9] Association between serum amyloid a proteins and coronary artery disease - Evidence from two distinct arteriosclerotic processes
Fyfe, AI
Rothenberg, LS
DeBeer, FC
Cantor, RM
Rotter, JI
Lusis, AJ
[J]. CIRCULATION, 1997, 96 (09) : 2914 - 2919
[10] MCP-1 deficiency reduces susceptibility to atherosclerosis in mice that overexpress human apolipoprotein B
Gosling, J
Slaymaker, S
Gu, L
Tseng, S
Zlot, CH
Young, SG
Rollins, BJ
Charo, IF
[J]. JOURNAL OF CLINICAL INVESTIGATION, 1999, 103 (06) : 773 - 778

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