Paraoxonase-1 inhibits oxidised LDL-induced MCP-1 production by endothelial cells

被引：162

作者：

Mackness, B ^{[1
]}

Hine, D ^{[1
]}

Liu, YF ^{[1
]}

Mastorikou, M ^{[1
]}

Mackness, M ^{[1
]}

机构：

[1] Manchester Royal Infirm, Dept Med, Manchester M13 9WL, Lancs, England

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2004年 / 318卷 / 03期

关键词：

paraoxonase-1; HDL; MCP-1; oxidation; endothelial cells;

D O I：

10.1016/j.bbrc.2004.04.056

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：

The upregulation of endothelial cell MCP-1 production by ox-LDL is a major initiating event in atherogenesis. HDL and PON1 retard the oxidation of LDL and therefore may retard endothelial cell MCP-1 production. The endothelial cell line EAhy926 was incubated with ox-LDL in the presence and absence of HDL and PON1 and the production of MCP-1 was measured by ELISA. Human HDL and PON1 significantly inhibited the in vitro oxidation of LDL and completely prevented the ox-LDL induced increase in MCP-1 production by endothelial cells. Ostrich HDL that does not contain PON1 was unable to prevent LDL-oxidation or the production of MCP-1 by endothelial cells. PON1 attenuates the ox-LDL induced MCP-1 production by endothelial cells. This is one, early, mechanism by which PON1 may be anti-atherogenic. (C) 2004 Elsevier Inc. All rights reserved.

引用

页码：680 / 683

页数：4

共 27 条

[1] Paraoxonase-1 reduces monocyte chemotaxis and adhesion to endothelial cells due to oxidation of palmitoyl, linoleoyl glycerophosphorylcholine [J].

Ahmed, Z ;

Babaei, S ;

Maguire, GF ;

Draganov, D ;

Kuksis, A ;

La Du, BN ;

Connelly, PW .

CARDIOVASCULAR RESEARCH, 2003, 57 (01) :225-231

[2] Apolipoprotein A-I promotes the formation of phosphatidylcholine core aldehydes that are hydrolyzed by paraoxonase (PON-1) during high density lipoprotein oxidation with a peroxynitrite donor [J].

Ahmed, Z ;

Ravandi, A ;

Maguire, GF ;

Emili, A ;

Draganov, D ;

La Du, BN ;

Kuksis, A ;

Connelly, PW .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (27) :24473-24481

[3] Human serum paraoxonases (PON1) Q and R selectively decrease lipid peroxides in human coronary and carotid atherosclerotic lesions - PON1 esterase and peroxidase-like activities [J].

Aviram, M ;

Hardak, E ;

Vaya, J ;

Mahmood, S ;

Milo, S ;

Hoffman, A ;

Billicke, S ;

Draganov, D ;

Rosenblat, M .

CIRCULATION, 2000, 101 (21) :2510-2517

[4] APPLICATION OF AN IMMORTALIZED HUMAN ENDOTHELIAL-CELL LINE TO THE LEUKOCYTE - ENDOTHELIAL ADHERENCE ASSAY [J].

BROWN, KA ;

VORA, A ;

BIGGERSTAFF, J ;

EDGELL, CJS ;

OIKLE, S ;

MAZURE, G ;

TAUB, N ;

MEAGER, A ;

HILL, T ;

WATSON, C ;

DUMONDE, DC .

JOURNAL OF IMMUNOLOGICAL METHODS, 1993, 163 (01) :13-22

[5]

Brushia RJ, 2001, J LIPID RES, V42, P951

[6] Elevated soluble cellular adhesion molecules in subjects with low HDL-cholesterol [J].

Calabresi, L ;

Gomaraschi, M ;

Villa, B ;

Omoboni, L ;

Dmitrieff, C ;

Franceschini, G .

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2002, 22 (04) :656-661

[7] Time sequence of the inhibition of endothelial adhesion molecule expression by reconstituted high density lipoproteins [J].

Clay, MA ;

Pyle, DH ;

Rye, KA ;

Vadas, MA ;

Gamble, JR ;

Barter, PJ .

ATHEROSCLEROSIS, 2001, 157 (01) :23-29

[8] HIGH-DENSITY-LIPOPROTEINS INHIBIT CYTOKINE-INDUCED EXPRESSION OF ENDOTHELIAL-CELL ADHESION MOLECULES [J].

COCKERILL, GW ;

RYE, KA ;

GAMBLE, JR ;

VADAS, MA ;

BARTER, PJ .

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1995, 15 (11) :1987-1994

[9] High density lipoproteins reduce organ injury and organ dysfunction in a rat model of hemorrhagic shock [J].

Cockerill, GW ;

McDonald, MC ;

Mota-Filipe, H ;

Cuzzocrea, S ;

Miller, NE ;

Thiemermann, C .

FASEB JOURNAL, 2001, 15 (11) :1941-1952

[10]

Cockerill GW, 2001, CIRCULATION, V103, P108

← 1 2 3 →