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Accepted Preprint first posted online on 8 May 2009

Journal of Endocrinology 2009;202:199.

Journal of Endocrinology (2009) In press
DOI: 10.1677/JOE-08-0363
© 2009 Society for Endocrinology
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RESEARCH

Angiotensin II Enhances the Increase in MCP-1 Production Induced by TNF-{alpha} from 3T3-L1 Preadipocytes

 Sachie Asamizu, Masaharu Urakaze, Chikaaki Kobashi, Manabu Ishiki, Amal Khalifa Norel Din, Shiho Fujisaka, Yukiko Kanatani, Agussalim Bukahari, Satoko Senda, Hikari Suzuki, Yuh Yamazaki, Minoru Iwata, Isao Usui, Katsuya Yamazaki, Hiroshi Ogawa, Masashi Kobayashi and Kazuyuki Tobe

S Asamizu, toyama, Japan
M Urakaze, Toyama, 930-0194, Japan
C Kobashi, Toyama, Japan
M Ishiki, toyama, Japan
A Norel Din, toyama, Japan
S Fujisaka, toyama, Japan
Y Kanatani, toyama, Japan
A Bukahari, toyama, Japan
S Senda, toyama, Japan
H Suzuki, toyama, Japan
Y Yamazaki, toyama, Japan
M Iwata, toyama, Japan
I Usui, toyama, Japan
K Yamazaki, toyama, Japan
H Ogawa, toyama, Japan
M Kobayashi, toyama, Japan
K Tobe, toyama, Japan

Correspondence: Masaharu Urakaze, Email: murakaze{at}med.u-toyama.ac.jp

Monocyte chemoattractant protein-1 (MCP-1) and Angiotensin II in adipose tissue have been revealed 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 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-dependently. Then, we examined the effect of Ang II and/or TNF-{alpha} on phosphorylation of 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 pathway probably due to AP-1 activation.






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