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作者

Zheng Zhang Shenwei Zhang Yong Wang Ming Yang Ning Zhang Zhitao Jin Liping Ding Wei Jiang Junke Yang Zhimin Sun Chunguang Qiu Taohong Hu

作者单位

The General Hospital of the PLA Rocket Force The Seventh People’s Hospital of Zhengzhou The Affiliate Hospital of Military Medicine Academy Taishan Medical University Shanghai Jiao Tong University Affiliated Sixth People’s Hospital

刊名

Apoptosis

关键词

Cardiac microvascular endothelial cells Autophagy mTOR Apoptosis High glucose

摘要

Cardiac microvascular endothelial cells (CMECs) dysfunction is an important pathophysiological event in the cardiovascular complications induced by diabetes. However, the underlying mechanism is not fully clarified. Autophagy is involved in programmed cell death. Here we investigated the potential role of autophagy on the CMECs injury induced by high glucose. CMECs were cultured in normal or high glucose medium for 6, 12 and 24 h respectively. The autophagy of CMECs was measured by green fluores...更多

Cardiac microvascular endothelial cells (CMECs) dysfunction is an important pathophysiological event in the cardiovascular complications induced by diabetes. However, the underlying mechanism is not fully clarified. Autophagy is involved in programmed cell death. Here we investigated the potential role of autophagy on the CMECs injury induced by high glucose. CMECs were cultured in normal or high glucose medium for 6, 12 and 24 h respectively. The autophagy of CMECs was measured by green fluorescence protein (GFP)-LC3 plasmid transfection. Moreover, the apoptosis of CMEC was determined by flow cytometry. Furthermore, 3-Methyladenine (3MA), ATG7 siRNA and rapamycin were administrated to regulate the autophagy state. Moreover, Western blotting assay was performed to measure the expressions of Akt, mTOR, LC3 and p62. High glucose stress decreased the autophagy, whereas increased the apoptosis in CMECs time dependently. Meanwhile, high glucose stress activated the Akt/mTOR signal pathway. Furthermore, autophagy inhibitor, 3-MA and ATG7 siRNA impaired the autophagy and increased the apoptosis in CMECs induced by high glucose stress. Conversely, rapamycin up-regulated the autophagy and decreased the apoptosis in CMECs under high glucose condition. Our data provide evidence that high glucose directly inhibits autophagy, as a beneficial adaptive response to protect CMECs against apoptosis. Furthermore, the autophagy was mediated, at least in part, by mTOR signaling.收起

学科

【SCI学科】CELL BIOLOGY;BIOCHEMISTRY & MOLECULAR BIOLOGY 【ESI学科】MOLECULAR BIOLOGY & GENETICS

影响因子

2016年:3.833;2015年:3.592;2014年:3.685;2013年:3.614;2012年:3.949

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