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Myocyte enhancer factor 2A delays vascular endothelial cell senescence by activating the PI3K/p-Akt/SIRT1 pathway

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机构： [1]Guangzhou Institute of Cardiovascular Disease, Guangdong Key Laboratory of Vascular Diseases, State Key Laboratory of Respiratory Disease, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510260, P. R. China [2]Department of Laboratory Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510120, P. R. China [3]Department of Emergency, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510260, P. R. China

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关键词： myocyte enhancer factor 2A Phosphatidylinositol-4 5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) 5-bisphosphate 3-kinase catalytic subunit gamma (PIK3CG) Sirtuin 1 (SIRT1) senescence

摘要：

Myocyte enhancer factor 2A (MEF2A) dysfunction is closely related to the occurrence of senile diseases such as cardiocerebro vascular diseases, but the underlying molecular mechanism is unclear. Here, we studied the effects of MEF2A on the senescent phenotype of vascular endothelial cells (VEC) and downstream signaling pathway, and the association between plasma MEF2A levels and coronary artery disease (CAD). Results showed that MEF2A silencing promoted cell senescence and down-regulated PI3K/p-AKT/Sirtuin 1 (SIRT1) expression. MEF2A overexpression delayed cell senescence and up-regulated PI3K/p-AKT/SIRT1. Hydrogen peroxide (H2O2) treatment induced cellular senescence and down-regulated the expression of MEF2A and PI3K/p-AKT/SIRT1. MEF2A overexpression inhibited cellular senescence and the down-regulation of PI3K/p-AKT/SIRT1 induced by H2O2. Further study revealed that MEF2A directly up-regulated the expression of PIK3CA and PIK3CG through MEF2 binding sites in the promoter region. Pearson correlation and logistic regression analysis showed that the plasma level of MEF2A was negatively correlated with CAD, and with age in the controls. These results suggested that MEF2A can directly up-regulate PI3K gene expression, and one of the molecular mechanisms of delaying effect of MEF2A on VEC cell senescence was SIRT1-expression activation through the PI3K/p-Akt pathway. Moreover, the plasma MEF2A levels may be a potential biomarker for CAD risk prediction.

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出版当年[2018]版：

大类 | 2 区生物

小类 | 2 区老年医学 3 区细胞生物学

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无

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出版当年[2017]版：

Q1 GERIATRICS & GERONTOLOGY Q2 CELL BIOLOGY

最新[2023]版：

Q2 CELL BIOLOGY Q2 GERIATRICS & GERONTOLOGY

影响因子： 3.9 最新[2023版] 4.9 最新五年平均 5.179 出版当年[2017版] 5.437 出版当年五年平均 4.867 出版前一年[2016版] 5.515 出版后一年[2018版]

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第一作者机构： [1]Guangzhou Institute of Cardiovascular Disease, Guangdong Key Laboratory of Vascular Diseases, State Key Laboratory of Respiratory Disease, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510260, P. R. China

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