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Angiotensin II enhances the increase in monocyte chemoattractant protein-1 production induced by tumor necrosis factor-{alpha} from 3T3-L1 preadipocytes.
J Endocrinol. 2009 Aug; 202(2):199-205.JE

Abstract

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.

Authors+Show Affiliations

1st Department of Medicine, Toyama University, Sugitani 2630, Toyama-shi 930-0194, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

19429670

Citation

Asamizu, Sachie, et al. "Angiotensin II Enhances the Increase in Monocyte Chemoattractant Protein-1 Production Induced By Tumor Necrosis Factor-{alpha} From 3T3-L1 Preadipocytes." The Journal of Endocrinology, vol. 202, no. 2, 2009, pp. 199-205.
Asamizu S, Urakaze M, Kobashi C, et al. Angiotensin II enhances the increase in monocyte chemoattractant protein-1 production induced by tumor necrosis factor-{alpha} from 3T3-L1 preadipocytes. J Endocrinol. 2009;202(2):199-205.
Asamizu, S., Urakaze, M., Kobashi, C., Ishiki, M., Norel Din, A. K., Fujisaka, S., Kanatani, Y., Bukahari, A., Senda, S., Suzuki, H., Yamazaki, Y., Iwata, M., Usui, I., Yamazaki, K., Ogawa, H., Ogawa, H., Kobayashi, M., & Tobe, K. (2009). Angiotensin II enhances the increase in monocyte chemoattractant protein-1 production induced by tumor necrosis factor-{alpha} from 3T3-L1 preadipocytes. The Journal of Endocrinology, 202(2), 199-205. https://doi.org/10.1677/JOE-08-0363
Asamizu S, et al. Angiotensin II Enhances the Increase in Monocyte Chemoattractant Protein-1 Production Induced By Tumor Necrosis Factor-{alpha} From 3T3-L1 Preadipocytes. J Endocrinol. 2009;202(2):199-205. PubMed PMID: 19429670.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Angiotensin II enhances the increase in monocyte chemoattractant protein-1 production induced by tumor necrosis factor-{alpha} from 3T3-L1 preadipocytes. AU - Asamizu,Sachie, AU - Urakaze,Masaharu, AU - Kobashi,Chikaaki, AU - Ishiki,Manabu, AU - Norel Din,Amal Khalifa, AU - Fujisaka,Shiho, AU - Kanatani,Yukiko, AU - Bukahari,Agussalim, AU - Senda,Satoko, AU - Suzuki,Hikari, AU - Yamazaki,Yuh, AU - Iwata,Minoru, AU - Usui,Isao, AU - Yamazaki,Katsuya, AU - Ogawa,Hirofumi, AU - Ogawa,Hiroshi, AU - Kobayashi,Masashi, AU - Tobe,Kazuyuki, Y1 - 2009/05/08/ PY - 2009/5/12/entrez PY - 2009/5/12/pubmed PY - 2009/9/22/medline SP - 199 EP - 205 JF - The Journal of endocrinology JO - J Endocrinol VL - 202 IS - 2 N2 - 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. SN - 1479-6805 UR - https://www.unboundmedicine.com/medline/citation/19429670/Angiotensin_II_enhances_the_increase_in_monocyte_chemoattractant_protein_1_production_induced_by_tumor_necrosis_factor_{alpha}_from_3T3_L1_preadipocytes_ L2 - https://joe.bioscientifica.com/doi/10.1677/JOE-08-0363 DB - PRIME DP - Unbound Medicine ER -