Angiotensin II enhances the increase in monocyte chemoattractant protein-1 production induced by tumor necrosis factor-α from 3T3-L1 preadipocytes

被引：15

作者：

Asamizu, Sachie ^{[1
]}

Urakaze, Masaharu ^{[1
]}

Kobashi, Chikaaki ^{[1
]}

Ishiki, Manabu ^{[1
]}

Din, Amal Khalifa Norel ^{[1
]}

Fujisaka, Shiho ^{[1
]}

Kanatani, Yukiko ^{[1
]}

Bukahari, Agussalim ^{[1
]}

Senda, Satoko ^{[1
]}

Suzuki, Hikari ^{[1
]}

Yamazaki, Yuh ^{[1
]}

Iwata, Minoru ^{[1
]}

Usui, Isao ^{[1
]}

Yamazaki, Katsuya ^{[1
]}

Ogawa, Hiroshi ^{[1
]}

Kobayashi, Masashi ^{[1
]}

Tobe, Kazuyuki ^{[1
]}

机构：

[1] Toyama Univ, Dept Med 1, Toyama 9300194, Japan

来源：

JOURNAL OF ENDOCRINOLOGY | 2009年 / 202卷 / 02期

关键词：

HUMAN ADIPOSE-TISSUE; INSULIN-RESISTANCE; HUMAN ADIPOCYTES; KAPPA-B; OBESITY; EXPRESSION; SYSTEM; INFLAMMATION; RELEASE; OVEREXPRESSION;

D O I：

10.1677/JOE-08-0363

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Monocyte chemoattractant protein-1 (MCP-1) and angiotensin It (Ang II) in adipose tissue are thought to induce systemic insulin resistance in rodents; but the precise mechanism is not fully clarified. We examined the mechanism of Ang II-induced and/or tumor necrosis factor-alpha (TNF-alpha)-induced MCP-1 production from 3T3-L1 preadipocytes. The MCP-1 protein and MCP-1 mRNA expression in 3T3-L1 preadipocytes were increased significantly by stimulation with TNF-alpha. We found no significant increase in MCP-1 concentrations by Ang II alone; but it enhanced the TNF-alpha-induced MCP-1 mRNA expression in a dose-dependent manner. Then, we examined the effect of Ang II and/or TNF-alpha on phosphorylation of extracellular signal-regulated kinase (ERK), p38MAPK, and I kappa B-alpha. Ang II and TNF-alpha clearly enhanced ERK and p38MAPK phosphorylation. I kappa B-alpha phosphorylation was enhanced by TNF-alpha, but not by Ang II. The MCP-1 mRNA expression induced by TNF-alpha and co-stimulation with Ang II was inhibited by either ERK inhibitor, p38MAPK inhibitor or NF-kappa B inhibitor. Moreover, Ang II enhanced the activation of AP-1 (c-fos) induced by TNF-alpha. Our results suggest that Ang II may serve as an additional Stimulus On the TNF-alpha-induced MCP-1 production through the ERK- and p38MAPK-dependent pathways probably due to AP-1 activation. Journal of Endocrinology (2009) 202, 199-205

引用

页码：199 / 205

页数：7

共 32 条

[1] Distinct signaling pathways for MCP-1-dependent integrin activation and chemotaxis [J].