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Cited by 346

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 access
Lee, Ji-Hyun, Song, Mi-Young, Song, Eun-Kyung, Kim, Eun-Kyung, Moon, Woo Sung, Han, Myung-Kwan, Park, Jin-Woo, Kwon, Kang-Beom, Park, Byung-Hyun·2009·Diabetes
DOI 10.2337/db07-1795
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Abstract

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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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
DOI
10.2337/db07-1795
OpenAlex
W2128737073
Cited by
346
References
41
FWCI
8.60
Type
journal article
Language
en
Open access
hybrid

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