| Literature DB >> 29967177 |
Huina Zhang1,2,3,4,5, Jian Liu3,4,5, Dan Qu3,4,5, Li Wang3,4,5, Chi Ming Wong3,4,5, Chi-Wai Lau3,4,5, Yuhong Huang3,4,5, Yi Fan Wang3,4,5, Huihui Huang6, Yin Xia6, Li Xiang7, Zongwei Cai7, Pingsheng Liu8, Yongxiang Wei9,2, Xiaoqiang Yao3,4,5, Ronald Ching Wan Ma10, Yu Huang11,4,5.
Abstract
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/db SExos-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.Entities:
Keywords: arginase 1; diabetes; endothelium; exosome; nitric oxide
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Year: 2018 PMID： 29967177 PMCID： PMC6055191 DOI： 10.1073/pnas.1721521115
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN： 0027-8424 Impact factor: 11.205