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Sirt1 hyperexpression in SHR heart related to left ventricular hypertrophy.
Li, Ling; Zhao, Lei; Yi-Ming, Wuliya; Yu, Yong-Sheng; Xia, Chun-Yan; Duan, Jun-Li; Su, Ding-Feng.
Afiliación
  • Li L; Department of Pharmacology, College of Pharmacy, Second Military Medical University, 325 Guo He Road, Shanghai 200433, China.
Can J Physiol Pharmacol ; 87(1): 56-62, 2009 Jan.
Article en En | MEDLINE | ID: mdl-19142216
Sirt1 is a human homologue of the silent information regulator factor 2 (Sir2) and has an NAD+-dependent histone deacetylase activity. This protein is reported to have a pathogenetic role in muscle differentiation, diabetic nephropathy, and heart failure. In this study, we investigated the expression of sirt1 in spontaneously hypertensive rat (SHR) to obtain insight into the function of sirt1 in hypertensive cardiovascular hypertrophy. The gene and protein expression of sirt1 was increased in the heart in SHR compared with normotensive WKY rats. Sirt1 mRNA was not different in the aorta between SHR and WKY rats. Sirt1 mRNA expression in heart and aorta was not related to hemodynamic parameters in SHR. Hypertensive left ventricular hypertrophy was significantly and positively related to the expression of heart tissue sirt1 mRNA in SHR. Aortic hypertrophy, however, was not related to sirt1 mRNA in the aorta. The increased sirt1 protein expression was accompanied by severe cardiac hypertrophy in older SHR. These results suggest that the increase of sirt1 gene and protein expression in the heart was associated with cardiac hypertrophy.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Hipertrofia Ventricular Izquierda / Sirtuinas Límite: Animals Idioma: En Revista: Can J Physiol Pharmacol Año: 2009 Tipo del documento: Article País de afiliación: China Pais de publicación: Canadá

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Hipertrofia Ventricular Izquierda / Sirtuinas Límite: Animals Idioma: En Revista: Can J Physiol Pharmacol Año: 2009 Tipo del documento: Article País de afiliación: China Pais de publicación: Canadá