PMID- 19429670 OWN - NLM STAT- MEDLINE DCOM- 20090921 LR - 20091119 IS - 1479-6805 (Electronic) IS - 0022-0795 (Linking) VI - 202 IP - 2 DP - 2009 Aug TI - Angiotensin II enhances the increase in monocyte chemoattractant protein-1 production induced by tumor necrosis factor-alpha from 3T3-L1 preadipocytes. PG - 199-205 LID - 10.1677/JOE-08-0363 [doi] AB - Monocyte chemoattractant protein-1 (MCP-1) and angiotensin II (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 IkappaB-alpha. Ang II and TNF-alpha clearly enhanced ERK and p38MAPK phosphorylation. IkappaB-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-kappaB 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. FAU - Asamizu, Sachie AU - Asamizu S AD - 1st Department of Medicine, Toyama University, Sugitani 2630, Toyama-shi 930-0194, Japan. FAU - Urakaze, Masaharu AU - Urakaze M FAU - Kobashi, Chikaaki AU - Kobashi C FAU - Ishiki, Manabu AU - Ishiki M FAU - Norel Din, Amal Khalifa AU - Norel Din AK FAU - Fujisaka, Shiho AU - Fujisaka S FAU - Kanatani, Yukiko AU - Kanatani Y FAU - Bukahari, Agussalim AU - Bukahari A FAU - Senda, Satoko AU - Senda S FAU - Suzuki, Hikari AU - Suzuki H FAU - Yamazaki, Yuh AU - Yamazaki Y FAU - Iwata, Minoru AU - Iwata M FAU - Usui, Isao AU - Usui I FAU - Yamazaki, Katsuya AU - Yamazaki K FAU - Ogawa, Hirofumi AU - Ogawa H FAU - Kobayashi, Masashi AU - Kobayashi M FAU - Tobe, Kazuyuki AU - Tobe K LA - eng PT - Journal Article DEP - 20090508 PL - England TA - J Endocrinol JT - The Journal of endocrinology JID - 0375363 RN - 0 (Chemokine CCL2) RN - 0 (RNA, Messenger) RN - 0 (Transcription Factor AP-1) RN - 0 (Tumor Necrosis Factor-alpha) RN - 11128-99-7 (Angiotensin II) RN - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases) RN - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1) RN - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3) RN - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases) SB - IM EIN - J Endocrinol. 2009 Oct;203(1):189. Ogawa, Hiroshi [corrected to Ogawa, Hirofumi] MH - 3T3-L1 Cells MH - Adipocytes/drug effects/*metabolism MH - Angiotensin II/*pharmacology MH - Animals MH - Chemokine CCL2/*biosynthesis/genetics MH - Drug Synergism MH - Enzyme Activation/drug effects MH - Extracellular Signal-Regulated MAP Kinases MH - Mice MH - Mitogen-Activated Protein Kinase 1/metabolism MH - Mitogen-Activated Protein Kinase 3/metabolism MH - RNA, Messenger/biosynthesis MH - Signal Transduction MH - Stem Cells/drug effects/*metabolism MH - Transcription Factor AP-1/metabolism MH - Tumor Necrosis Factor-alpha/*pharmacology MH - p38 Mitogen-Activated Protein Kinases/metabolism EDAT- 2009/05/12 09:00 MHDA- 2009/09/22 06:00 CRDT- 2009/05/12 09:00 PHST- 2009/05/12 09:00 [entrez] PHST- 2009/05/12 09:00 [pubmed] PHST- 2009/09/22 06:00 [medline] AID - JOE-08-0363 [pii] AID - 10.1677/JOE-08-0363 [doi] PST - ppublish SO - J Endocrinol. 2009 Aug;202(2):199-205. doi: 10.1677/JOE-08-0363. Epub 2009 May 8.