13
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Extracellular vesicles derived from human bone marrow mesenchymal stem cells promote angiogenesis in a rat myocardial infarction model.

      Journal of Molecular Medicine (Berlin, Germany)
      Animals, Cell Hypoxia, Cell Movement, Cell Proliferation, Cells, Cultured, Coronary Vessels, physiopathology, Exosomes, physiology, Human Umbilical Vein Endothelial Cells, metabolism, Humans, Male, Mesenchymal Stromal Cells, Myocardial Infarction, therapy, Neovascularization, Physiologic, Rats, Wistar, Secretory Vesicles, Stroke Volume, Ventricular Function, Left

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Mesenchymal stem cells (MSCs) have been increasingly tested experimentally and clinically for cardiac repair. However, the underlying mechanisms remain controversial due to the poor viability and considerable death of the engrafted cells in the infracted myocardium. Recent reports have suggested that extracellular vesicles (EVs) released by MSCs have angiogenesis-promoting activity; however, the therapeutic effect of MSC-EVs on an ischemic heart is unclear. In the present study, we reported that MSCs could release a large quantity of EVs around 100 nm in diameter upon hypoxia stimulation though the majority of the cells had not experienced apoptosis. MSC-EVs could be promptly uptaken by human umbilical vein endothelial cells, and the internalization resulted in dose-dependent enhancement of in vitro proliferation, migration, and tube formation of endothelial cells. Using an acute myocardial infarction rat model, we found that intramyocardial injection of MSC-EVs markedly enhanced blood flow recovery, in accordance with reduced infarct size and preserved cardiac systolic and diastolic performance compared to those treated with PBS. These data suggest that like MSCs, MSC-EVs could also protect cardiac tissue from ischemic injury at least by means of promoting blood vessel formation, though further detailed investigations should be performed to define the functionality of MSC-EVs. MSCs released extracellular vesicles (EVs) upon hypoxia stimulation. MSC-EVs were a mixture of microvesicles and exosomes. MSC-EVs could be promptly uptaken by human umbilical vein endothelial cells. MSC-EVs promoted neoangiogenesis in vitro and in vivo. MSC-EVs preserved cardiac performance in an AMI model.

          Related collections

          Author and article information

          Comments

          Comment on this article