首页 / 院系成果 / 成果详情页

Sitagliptin-mediated preservation of endothelial progenitor cell function via augmenting autophagy enhances ischaemic angiogenesis in diabetes 期刊论文

编号：

96052edc-b67e-4f6d-a1a3-bc84d1eb0790
作者：

Dai, Xiaozhen#^[1,2,3]Zeng, Jun#^[3,4]Yan, Xiaoqing^[1];Lin, Qian^[3,5];Wang, Kai^[3,6,7,8];Chen, Jing^[3];Shen, Feixia^[6,7,8];Gu, Xuemei^[6,7,8];Wang, Yuehui(王越晖)^[9]Chen, Jun^[1,3];Pan, Kejian^[2];Cai, Lu^[1,3,5];Wintergerst, Kupper A.^[10];Tan, Yi(谭毅)*^[1,3,5]
语种：

英文
期刊：

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE ISSN：1582-4934 2018 年 22 卷 1 期 (89 - 100) ; JAN
收录：
关键词：

sitagliptin angiogenesis hind limb ischaemia endothelial progenitor cells autophagy
摘要：

Recently, the dipeptidyl peptidase-4 (DPP-4) inhibitor sitagliptin, a major anti-hyperglycaemic agent, has received substantial attention as a therapeutic target for cardiovascular diseases via enhancing the number of circulating endothelial progenitor cells (EPCs). However, the direct effects of sitagliptin on EPC function remain elusive. In this study, we evaluated the proangiogenic effects of sitagliptin on a diabetic hind limb ischaemia (HLI) model in vivo and on EPC culture in vitro. Treatment of db/db mice with sitagliptin (Januvia) after HLI surgery efficiently enhanced ischaemic angiogenesis and blood perfusion, which was accompanied by significant increases in circulating EPC numbers. EPCs derived from the bone marrow of normal mice were treated with high glucose to mimic diabetic hyperglycaemia. We found that high glucose treatment induced EPC apoptosis and tube formation impairment, which were significantly prevented by sitagliptin pretreatment. A mechanistic study found that high glucose treatment of EPCs induced dramatic increases in oxidative stress and apoptosis; pretreatment of EPCs with sitagliptin significantly attenuated high glucose-induced apoptosis, tube formation impairment and oxidative stress. Furthermore, we found that sitagliptin restored the basal autophagy of EPCs that was impaired by high glucose via activating the AMP-activated protein kinase/unc-51-like autophagy activating kinase 1 signalling pathway, although an autophagy inhibitor abolished the protective effects of sitagliptin on EPCs. Altogether, the results indicate that sitagliptin-induced preservation of EPC angiogenic function results in an improvement of diabetic ischaemia angiogenesis and blood perfusion, which are most likely mediated by sitagliptin-induced prevention of EPC apoptosis via augmenting autophagy.
推荐引用方式
GB/T 7714：

Dai Xiaozhen,Zeng Jun,Yan Xiaoqing, et al. Sitagliptin-mediated preservation of endothelial progenitor cell function via augmenting autophagy enhances ischaemic angiogenesis in diabetes [J].JOURNAL OF CELLULAR AND MOLECULAR MEDICINE,2018,22(1):89-100.
APA：

Dai Xiaozhen,Zeng Jun,Yan Xiaoqing,Lin Qian,&Tan Yi.(2018).Sitagliptin-mediated preservation of endothelial progenitor cell function via augmenting autophagy enhances ischaemic angiogenesis in diabetes .JOURNAL OF CELLULAR AND MOLECULAR MEDICINE,22(1):89-100.
MLA：

Dai Xiaozhen, et al. "Sitagliptin-mediated preservation of endothelial progenitor cell function via augmenting autophagy enhances ischaemic angiogenesis in diabetes" .JOURNAL OF CELLULAR AND MOLECULAR MEDICINE 22,1(2018):89-100.
条目包含文件：

文件类型：PDF,文件大小：

正在加载全文

未找到全文

浏览次数：57  下载次数：0

分享到：

浏览次数：57

下载次数：0

打印次数：0