期刊
CIRCULATION RESEARCH
卷 95, 期 9, 页码 902-910出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/01.RES.0000146947.84294.4c
关键词
eNOS; redox; hypertension; H-ras
资金
- NHLBI NIH HHS [HL70929, HL65608] Funding Source: Medline
- NIA NIH HHS [AG021523] Funding Source: Medline
The dual-function protein apurinic/apyrmidinic endonuclease/redox factor-1 (APE1/ref-1) is essential for DNA repair and also governs the reductive activation of many redox-sensitive transcription factors. We examined the role of APE1/ref-1 in regulation of endothelium-dependent tone and systemic blood pressure. APE1/ref-1(+/-) mice have impaired endothelium-dependent vasorelaxation, reduced vascular NO levels, and are hypertensive. APE1/ref-1 upregulates H-ras expression and leads to H-ras-mediated, phosphoinositide-3 kinase/Akt kinase-dependent calcium sensitization of endothelial NO synthase (eNOS), stimulating NO production. The reducing property of APE1/ref-1 is essential for upregulation of H-ras and for the calcium sensitization of eNOS. These findings uncover a novel physiological role for APE1/ref-1 in regulating vascular tone by governance of eNOS activity and bioavailable NO.
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