The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.
Overexpression of SIRT1 Protects Pancreatic β-Cells Against Cytokine Toxicity by Suppressing the Nuclear Factor-κB Signaling Pathway
Open accessAbstract
OBJECTIVE—SIRT1, a class III histone/protein deacetylase, is known to interfere with the nuclear factor-κB (NF-κB) signaling pathway and thereby has an anti-inflammatory function. Because of the central role of NF-κB in cytokine-mediated pancreatic β-cell damage, we postulated that SIRT1 might work in pancreatic β-cell damage models. RESEARCH DESIGN AND METHODS—RINm5F (RIN) cells or isolated rat islets were treated with interleukin-1β and interferon-γ. SIRT1 was activated by resveratrol, a pharmacological activator, or ectopic overexpression. The underlying mechanisms of SIRT1 against cytokine toxicity were further explored. RESULTS—Treatment of RIN cells with cytokines induced cell damage, and this damage was well correlated with the expression of the inducible form of nitric oxide (NO) synthase (iNOS) and NO production. However, SIRT1 overexpression completely prevented cytokine-mediated cytotoxicity, NO production, and iNOS expression. The molecular mechanism by which SIRT1 inhibits iNOS expression appeared to involve the inhibition of the NF-κB signaling pathway through deacetylation of p65. In addition, SIRT1 activation by either resveratrol or adenoviral-directed overexpression of SIRT1 could prevent cytokine toxicity and maintain normal insulin-secreting responses to glucose in isolated rat islets. CONCLUSIONS—This study will provide valuable information not only into the mechanisms underlying β-cell destruction but also into the regulation of SIRT1 as a possible target to attenuate cytokine-induced β-cell damage.
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Cites
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Cited by
Kauppinen, A., Suuronen, T., Ojala, J., Kaarniranta, K., & Salminen, A. (2013) · Cellular Signalling · doi:10.1016/j.cellsig.2013.06.007 · Cited by 989
Mitohormesis: Promoting Health and Lifespan by Increased Levels of Reactive Oxygen Species (ROS)
Ristow, M., & Schmeisser, K. (2014) · Dose-Response · doi:10.2203/dose-response.13-035.ristow · Cited by 534
Liu, K., Zhou, R., Wang, B., & Mi, M.-T. (2014) · The American Journal of Clinical Nutrition · doi:10.3945/ajcn.113.082024 · Cited by 323
Sirt1 activation protects the mouse renal medulla from oxidative injury
He, W., Wang, Y., Zhang, M.-Z., You, L., Davis, L. S., Fan, H., Yang, H.-C., Fogo, A. B., Zent, R., Harris, R. C., et al. (2010) · Journal of Clinical Investigation · doi:10.1172/jci41563 · Cited by 317
Aging and disease: connections to sirtuins
Donmez, G., & Guarente, L. (2010) · Aging Cell · doi:10.1111/j.1474-9726.2010.00548.x · Cited by 311
Metadata
- Authors
- Lee, J.-H., Song, M.-Y., Song, E.-K., Kim, E.-K., Moon, W. S., Han, M.-K., Park, J.-W., Kwon, K.-B., & Park, B.-H.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2009-02-01
- Volume
- 58
- Issue
- 2
- Pages
- 344-351
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2128737073
- Cited by
- 346
- References
- 41
- FWCI
- 8.60
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Lee, J.-H., Song, M.-Y., Song, E.-K., Kim, E.-K., Moon, W. S., Han, M.-K., Park, J.-W., Kwon, K.-B., & Park, B.-H. (2009). Overexpression of SIRT1 Protects Pancreatic β-Cells Against Cytokine Toxicity by Suppressing the Nuclear Factor-κB Signaling Pathway. Diabetes. https://doi.org/10.2337/db07-1795
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