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      Myocardial reparative functions of exosomes from mesenchymal stem cells are enhanced by hypoxia treatment of the cells via transferring microRNA-210 in an nSMase2-dependent way

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          Abstract

          Hypoxia treatment enhances paracrine effect of mesenchymal stem cells (MSCs). The aim of this study was to investigate whether exosomes from hypoxia-treated MSCs (Exo H) are superior to those from normoxia-treated MSCs (Exo N) for myocardial repair. Mouse bone marrow-derived MSCs were cultured under hypoxia or normoxia for 24 h, and exosomes from conditioned media were intramyocardially injected into infarcted heart of C57BL/6 mouse. Exo H resulted in significantly higher survival, smaller scar size and better cardiac functions recovery. Exo H conferred increased vascular density, lower cardiomyocytes (CMs) apoptosis, reduced fibrosis and increased recruitment of cardiac progenitor cells in the infarcted heart relative to Exo N. MicroRNA analysis revealed significantly higher levels of microRNA-210 (miR-210) in Exo H compared with Exo N. Transfection of a miR-210 mimic into endothelial cells (ECs) and CMs conferred similar biological effects as Exo H. Hypoxia treatment of MSCs increased the expression of neutral sphingomyelinase 2 (nSMase2) which is crucial for exosome secretion. Blocking the activity of nSMase2 resulted in reduced miR-210 secretion and abrogated the beneficial effects of Exo H. In conclusion, hypoxic culture augments miR-210 and nSMase2 activities in MSCs and their secreted exosomes, and this is responsible at least in part for the enhanced cardioprotective actions of exosomes derived from hypoxia-treated cells.

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          Author and article information

          Journal
          101594777
          40767
          Artif Cells Nanomed Biotechnol
          Artif Cells Nanomed Biotechnol
          Artificial cells, nanomedicine, and biotechnology
          2169-1401
          2169-141X
          26 February 2018
          16 November 2017
          December 2018
          01 December 2018
          : 46
          : 8
          : 1659-1670
          Affiliations
          [a ]Department of Cardiology, Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, PR China
          [b ]Department of Cardiology, Cardiovascular Key Laboratory of Zhejiang Province, Hangzhou, PR China
          [c ]Department of Cardiology, The First People’s Hospital of Huzhou, Huzhou, PR China
          [d ]Vascular Biology Center, Department of Medicine, Medical College of Georgia/Georgia Regents University, Augusta, GA, USA
          [e ]Department of Molecular and Cellular Pharmacology, Leonard M. Miller School of Medicine, University of Miami, Miami, FL, USA
          Author notes
          CONTACT Hong Yu, yuvascular@ 123456zju.edu.cn , Department of Cardiology, Second Affiliated Hospital, College of Medicine, Zhejiang University, Cardiovascular Key Laboratory of Zhejiang Province, 88 Jiefang Rd, Hangzhou 310009, PR China
          [*]

          These authors contributed equally to this article.

          Article
          PMC5955787 PMC5955787 5955787 nihpa942418
          10.1080/21691401.2017.1388249
          5955787
          29141446
          807302e3-f369-4ec0-a5e7-fe909f15266e
          History
          Categories
          Article

          nSMase2,microRNA210,MSCs,hypoxia,Exosomes,myocardial infarction
          nSMase2, microRNA210, MSCs, hypoxia, Exosomes, myocardial infarction

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