Overexpressed eNOS upregulates SIRT1 expression and protects mouse pancreatic β cells from apoptosis

Abstract

Abstract. Loss of sirtuin 1 (SIRT1) activity may be associated with metabolic diseases, including diabetes. The aim of the present study was to investigate the potential effects of overexpressed endothelial nitric oxide synthase (eNOS) on cell proliferation and apoptosis with SIRT1 activation in the Min6 mouse pancreatic β cell line. A pcDNA3.0-eNOS plasmid was constructed and transfected into Min6 cells for 24 h prior to harvesting. eNOS expression was validated and SIRT1 expression was detected following plasmid transfection using reverse transcription-quantitative polymerase chain reaction and western blot analysis, which demonstrated that the expression levels of eNOS and SIRT1 were significantly upregulated. Furthermore, the cell proliferation and cell apoptosis of the Min6 cells were evaluated, using a cell counting kit-8 assay and flow cytometry, respectively. The results suggested that overexpressed eNOS promoted cell proliferation and inhibited cell apoptosis in Min6 cells. The interaction between eNOS and SIRT1 was explored through co-immunoprecipitation, and it found that there was a strong interaction between eNOS and SIRT1. In conclusion, overexpressed eNOS may induce SIRT1 activation, which is implied to play a protective role in Min6 cells, and eNOS may be a new therapeutic target for diseases such as type 2 diabetes.

The Role of Sirtuin1 in Regulating Endothelial Function, Arterial Remodeling and Vascular Aging

“…In cultured adipocyte, the SIRT1 expression is enhanced by treatments of NO donors and cGMP analogs (Nisoli et al, 2005). SIRT1 expression is also upregulated by overexpression of eNOS in the cultured mouse pancreatic β-cell line Min6 (Hu et al, 2017). These indicate the importance of eNOS-derived NO as a regulator of SIRT1 expression.…”

Buyang Huanwu Decoction Targets SIRT1/VEGF Pathway to Promote Angiogenesis After Cerebral Ischemia/Reperfusion Injury

“…Sirtuin 1 (SIRT1), a NAD + -dependent class III histone deacetylase, expresses in all cell types. It targets a wide range of transcription factors and consequently, is involved in many physiological and pathological processes as diverse as energy metabolism and myogenesis (Michan and Sinclair, 2007), oxidation-stress (Lee et al, 2018), inflammation (Velagapudi et al, 2017), and apoptosis (Hu T. et al, 2017). Recent studies (Potente et al, 2007; Ota et al, 2010) have demonstrated that SIRT1 is highly expressed in the vasculature during blood vessel growth and regulate the angiogenic activity of endothelial cells.…”

Exploring metabolic biomarkers and regulation pathways of acute pancreatitis using ultra-performance liquid chromatography combined with a mass spectrometry-based metabolomics strategy

“…24 At present, the release of inammatory factors promotes the apoptosis of pancreatic cells, and the reduction in the apoptosis of pancreatic cells aer AP has become one of the current research hotspots in many pathogenesis analyses of AP. 25,26 The selection of animal species and the method of model preparation play important roles in this type of research. A druginduced AP rat model is superior to a mouse model in terms of stability and the degree of pancreatic lesion homogeneity, and rats are also more convenient when it comes to monitoring hemodynamics and organ function.…”