Department of Nuclear Medicine, The Affiliate Hospital of Military Medicine Academy, Beijing, 100071, ChinaDepartment of Cardiology, The Seventh People’s Hospital of Zhengzhou, Zhengzhou, Henan 450016, ChinaShanghai Jiao Tong University Affiliated Sixth People’s Hospital, Shanghai, 201306, Chinaf Department of Outpatient, The General Hospital of the PLA Rocket Force, Beijing, 100088, ChinaSchool of Basic Medical Sciences, Taishan Medical University, Taian, Shandong 271000, Chinaa Department of Cardiology, The General Hospital of the PLA Rocket Force, Beijing, 100088, China
Cardiac microvascular endothelial cells 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 p...更多
Cardiac microvascular endothelial cells 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 -LC3 plasmid transfection. Moreover, the apoptosis of CMEC was determined by flow cytometry. Furthermore, 3-Methyladenine , 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
