title: Irisin Increased the Number and Improved the Function of Endothelial Progenitor Cells in Diabetes Mellitus Mice.
abstract: The dysfunction of endothelial progenitor cells (EPCs) was found to be associated with vascular complications in diabetes mellitus (DM) patients. Previous studies found that regular exercise could improve the function of EPCs in DM patients, but the underling mechanism was unclear. Irisin, a newly identified myokine, was induced by exercise and has been demonstrated to mediate some of the positive effects of exercise. In this study, we hypothesize that irisin may have direct effects on EPC function in DM mice. These data showed for the first time that irisin increased the number of EPCs in peripheral blood of DM mice and improved the function of EPCs derived from DM mice bone marrow. The mechanism for the effect of irisin is related to the PI3K/Akt/eNOS pathway. Furthermore, irisin was demonstrated to improve endothelial repair in DM mice that received EPC transplants after carotid artery injury. The results of this study indicate a novel effect of irisin in regulating the number and function of EPCs via the PI3K/Akt/eNOS pathway, suggesting a potential for the administration of exogenous irisin as a succedaneum to improve EPC function in diabetic patients who fail to achieve such improvements through regular exercise.
authors.affiliation: *Cell Biological Therapy Center of Kunming General Hospital, Chengdu Military Area Command of PLA, Cell Biological Medicine Integrated Engineering Laboratory of State and Region, Kunming, Yunnan Province, People's Republic of China; †Cardiovascular Institute of Xinqiao Hospital, Third Military Medical University, Chongqing, People's Republic of China; and ‡Department of Clinical Laboratory, PLA Kunming General Hospital Clinical College of Medicine, Kunming Medical University, Kunming, Yunnan Province, People's Republic of China.
authors.forename: Guangxu
authors.initials: G
authors.lastname: Zhu
authors.forename: Jinxiang
authors.initials: J
authors.lastname: Wang
authors.forename: Mingbao
authors.initials: M
authors.lastname: Song
authors.forename: Fang
authors.initials: F
authors.lastname: Zhou
authors.forename: Dagan
authors.initials: D
authors.lastname: Fu
authors.forename: Guangping
authors.initials: G
authors.lastname: Ruan
authors.forename: Xiangqing
authors.initials: X
authors.lastname: Zhu
authors.forename: Yinyin
authors.initials: Y
authors.lastname: Bai
authors.forename: Lan
authors.initials: L
authors.lastname: Huang
authors.forename: Rongqing
authors.initials: R
authors.lastname: Pang
authors.forename: Huali
authors.initials: H
authors.lastname: Kang
authors.forename: Xinghua
authors.initials: X
authors.lastname: Pan
mesh_terms: D000818:Animals; D002339:Carotid Arteries / Q000378:metabolism / Q000473:pathology; D020212:Carotid Artery Injuries / Q000378:metabolism / Q000473:pathology / Q000628:therapy; D002465:Cell Movement / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000378:metabolism; D066026:Endothelial Progenitor Cells / Q000187:drug effects* / Q000378:metabolism / Q000637:transplantation; D005353:Fibronectins / Q000494:pharmacology*; D008297:Male; D008810:Mice, Inbred C57BL; D058426:Neointima; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D058539:Phosphatidylinositol 3-Kinase / Q000378:metabolism; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects
chemical_list: C577593:FNDC5 protein, human; D005353:Fibronectins; D052250:Nitric Oxide Synthase Type III; C496315:Nos3 protein, mouse; D058539:Phosphatidylinositol 3-Kinase; D051057:Proto-Oncogene Proteins c-akt