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Serum exosomes mediate delivery of arginase 1 as a novel mechanism for endothelial dysfunction in diabetes

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收录情况： ◇ SCIE ◇ 自然指数

作者：

机构： [a]Beijing An Zhen Hospital, Capital Medical University, 100029 Beijing, China, [b]Key Laboratory of Upper Airway Dysfunction-related Cardiovascular Diseases, Beijing Institute of Heart Lung and Blood Vessel Disease, 100029 Beijing, China, [c]Shenzhen Research Institute, Chinese University of Hong Kong, Hong Kong, China, [d]Institute of Vascular Medicine, Chinese University of Hong Kong, Hong Kong, China, [e]Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Hong Kong, China, [f]School of Biomedical Sciences, Faculty of Medicine, Chinese University of Hong Kong, Hong Kong, China, [g]State Key Laboratory of Environmental and Biological Analysis, Department of Chemistry, Hong Kong Baptist University, Hong Kong, China, [h]National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, 100101 Beijing, China, [i]Department of Medicine and Therapeutics, Chinese University of Hong Kong, Hong Kong, China

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关键词： exosome arginase 1 endothelium nitric oxide diabetes

摘要：

Exosomes, abundant in blood, deliver various molecules to recipient cells. Endothelial cells are directly exposed to circulating substances. However, how endothelial cells respond to serum exosomes (SExos) and the implications in diabetes-associated vasculopathy have never been explored. In the present study, we showed that SExos from diabetic db/db mice (db/db SExos) were taken up by aortic endothelial cells, which severely impaired endothelial function in nondiabetic db/m(+) mice. The exosomal proteins, rather than RNAs, mostly account for db/dbSExos-induced endothelial dysfunction. Comparative proteomics analysis showed significant increase of arginase 1 in db/db SExos. Silence or overexpression of arginase 1 confirmed its essential role in db/db SExos-induced endothelial dysfunction. This study is a demonstration that SExos deliver arginase 1 protein to endothelial cells, representing a cellular mechanism during development of diabetic endothelial dysfunction. The results expand the scope of blood-borne substances that monitor vascular homeostasis.

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出版当年[2017]版：

大类 | 1 区

综合性期刊

小类 | 1 区综合性期刊

最新[2023]版：

大类 | 1 区

综合性期刊

小类 | 1 区综合性期刊

JCR分区：

出版当年[2016]版：

Q1 MULTIDISCIPLINARY SCIENCES

最新[2023]版：

Q1 MULTIDISCIPLINARY SCIENCES

影响因子： 9.4 最新[2023版] 10.8 最新五年平均 9.661 出版当年[2016版] 10.414 出版当年五年平均 9.423 出版前一年[2015版] 9.504 出版后一年[2017版]

第一作者：

第一作者机构： [a]Beijing An Zhen Hospital, Capital Medical University, 100029 Beijing, China, [b]Key Laboratory of Upper Airway Dysfunction-related Cardiovascular Diseases, Beijing Institute of Heart Lung and Blood Vessel Disease, 100029 Beijing, China, [c]Shenzhen Research Institute, Chinese University of Hong Kong, Hong Kong, China, [d]Institute of Vascular Medicine, Chinese University of Hong Kong, Hong Kong, China, [e]Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Hong Kong, China,

共同第一作者：

通讯作者：

通讯机构： [a]Beijing An Zhen Hospital, Capital Medical University, 100029 Beijing, China, [b]Key Laboratory of Upper Airway Dysfunction-related Cardiovascular Diseases, Beijing Institute of Heart Lung and Blood Vessel Disease, 100029 Beijing, China, [c]Shenzhen Research Institute, Chinese University of Hong Kong, Hong Kong, China, [d]Institute of Vascular Medicine, Chinese University of Hong Kong, Hong Kong, China, [e]Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Hong Kong, China,

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Serum exosomes mediate delivery of arginase 1 as a novel mechanism for endothelial dysfunction in diabetes

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