The effect of the expression of angiotensin II on extracellular matrix metalloproteinase inducer (EMMPRIN) in macrophages is mediated via the AT1/COX-2/PGE2 pathway

被引：15

作者：

Yang, Li-xia ^{[1
]}

Ye, Jin-shan ^{[1
]}

Guo, Rui-wei ^{[1
]}

Liu, Hong ^{[1
]}

Wang, Xian-mei ^{[1
]}

Qi, Feng ^{[1
]}

Guo, Chuanming ^{[1
]}

机构：

[1] Kunming Gen Hosp Chengdu Mil Area, Dept Cardiol, Yunnan 650032, Peoples R China

来源：

INFLAMMATION RESEARCH | 2010年 / 59卷 / 12期

关键词：

Angiotensin II; Macrophage; Extracellular matrix metalloproteinase inducer; Losartan; PGE(2); ATHEROSCLEROTIC LESION FORMATION; SMOOTH-MUSCLE-CELLS; E-DEFICIENT MICE; CARDIOVASCULAR EVENTS; PLAQUE INSTABILITY; CANCER-CELLS; CYCLOOXYGENASE-2; INHIBITION; DISEASE; TRIAL;

D O I：

10.1007/s00011-010-0223-3

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

To explore the expression of extracellular matrix metalloproteinase inducer (EMMPRIN) in THP-1 macrophages induced by angiotensin II (Ang II) and the mechanism of EMMPRIN expression. THP-1 cells were cultured and induced into macrophages, then stimulated with 10(-6) mol/L Ang II. Levels of EMMPRIN gene and its protein were measured by real-time polymerase chain reaction and western blotting. Prostaglandin E-2 (PGE(2)) expression was assayed by enzyme-linked immunosorbent assay. Antagonists of the angiotensin type-1 receptor (AT(1)R) and angiotensin type-2 receptor (AT(2)R) were used to inhibit the effect of Ang II, and PGE(2) added to detail the mechanism of Ang II-induced EMMPRIN expression. Ang II clearly induced the expression of EMMPRIN mRNA and protein in macrophages; this expression peaked at 12 h and declined after 24 h. The tendency of enhancement of the levels of cyclooxygenase-2 (COX-2) and PGE(2) was coincident with EMMPRIN expression. AT(1)-receptor antagonists and COX-2 inhibitors inhibited the effect of Ang II, but AT(2)-receptor antagonists did not. Ang II can up-regulate EMMPRIN expression in THP-1 macrophages via the AT(1)/COX-2/PGE(2) signal transduction pathway, and the effect can be inhibited by losartan and NS-398.

引用

页码：1033 / 1040

页数：8