The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
Repression of P66Shc Expression by SIRT1 Contributes to the Prevention of Hyperglycemia-Induced Endothelial Dysfunction
Open accessAbstract
Rationale: Inactivation of the p66Shc adaptor protein confers resistance to oxidative stress and protects mice from aging-associated vascular diseases. However, there is limited information about the negative regulating mechanisms of p66Shc expression in the vascular system. Objective: In this study, we investigated the role of SIRT1, a class III histone deacetylase, in the regulation of p66Shc expression and hyperglycemia-induced endothelial dysfunction. Methods and Results: Expressions of p66Shc gene transcript and protein were significantly increased by different kinds of class III histone deacetylase (sirtuin) inhibitors in human umbilical vein endothelial cells and 293A cells. Adenoviral overexpression of SIRT1 inhibited high-glucose–induced p66Shc upregulation in human umbilical vein endothelial cells. Knockdown of SIRT1 increased p66Shc expression and also increased the expression levels of plasminogen activator inhibitor-1 expression, but decreased manganese superoxide dismutase expression in high-glucose conditions. However, knockdown of p66Shc significantly reversed the effects of SIRT1 knockdown. In addition, p66Shc overexpression significantly decreased manganese superoxide dismutase expression and increased plasminogen activator inhibitor-1 expression in high-glucose conditions, which were recovered by SIRT1 overexpression. Moreover, compared to streptozotocin-induced wild-type diabetic mice, endothelium-specific SIRT1 transgenic diabetic mice had decreased p66Shc expression at both the mRNA and the protein levels, improved endothelial function, and reduced accumulation of nitrotyrosine and 8-OHdG (markers of oxidative stress). We further found that SIRT1 was able to bind to the p66Shc promoter (−508 bp to −250 bp), resulting in a decrease in the acetylation of histone H3 bound to the p66Shc promoter region. Conclusion: Our findings indicate that repression of p66Shc expression by SIRT1 contributes to the protection of hyperglycemia-induced endothelial dysfunction.
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Cites
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Cited by
Endothelial dysfunction and vascular disease - a 30th anniversary update
Vanhoutte, P. M., Shimokawa, H., Feletou, M., & Tang, E. H. C. (2017) · Acta Physiologica · doi:10.1111/apha.12646 · Cited by 937
The Aging Cardiovascular System
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Sirtuins, a promising target in slowing down the ageing process
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Calorie restriction and sirtuins revisited
Guarente, L. (2013) · Genes & Development · doi:10.1101/gad.227439.113 · Cited by 464
Metadata
- Authors
- Zhou, S., Chen, H.-Z., Wan, Y.-Z., Zhang, Q.-J., Wei, Y.-S., Huang, S., Liu, J.-J., Lu, Y.-B., Zhang, Z.-Q., Yang, R.-F., Zhang, R., Cai, H., Liu, D.-P., & Liang, C.-C.
- Venue
- Circulation Research
- Published
- 2011-09-02
- Volume
- 109
- Issue
- 6
- Pages
- 639-648
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2121808478
- Cited by
- 273
- References
- 13
- FWCI
- 9.22
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Zhou, S., Chen, H.-Z., Wan, Y.-Z., Zhang, Q.-J., Wei, Y.-S., Huang, S., Liu, J.-J., Lu, Y.-B., Zhang, Z.-Q., Yang, R.-F., Zhang, R., Cai, H., Liu, D.-P., & Liang, C.-C. (2011). Repression of P66Shc Expression by SIRT1 Contributes to the Prevention of Hyperglycemia-Induced Endothelial Dysfunction. Circulation Research. https://doi.org/10.1161/circresaha.111.243592
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