alexa Protective Role of Stem Cell Derived Extracellular Vesicles in an In Vitro Model of Hyperglycemia-Induced Endothelial Injury
ISSN: 2157-7013

Journal of Cell Science & Therapy
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Short Communication

Protective Role of Stem Cell Derived Extracellular Vesicles in an In Vitro Model of Hyperglycemia-Induced Endothelial Injury

Chiara Gai1, Yonathan Gomez1, Ciro Tetta2, Maria Felice Brizzi1,3 and Giovanni Camussi1*

1Department of Medical Sciences, University of Torino, Italy

2Unicyte AG, Oberdorf NW, Switzerland

32i3T, Society for the Management of Enterprise Incubator and the Technology Transfer, Scarl University of Torino, Italy

*Corresponding Author:
Giovanni Camussi
Department of Medical Sciences
University of Torino, Italy
Tel: +390116709588
Fax: +39 0116631184
E-mail: [email protected]

Received date: March 06, 2017; Accepted date: March 17, 2017; Published date: March 20, 2017

Citation: Gai C, Gomez Y, Tetta C, Brizzi MF, Camussi G (2017) Protective Role of Stem Cell Derived Extracellular Vesicles in an In Vitro Model of Hyperglycemia-Induced Endothelial Injury. J Cell Sci Ther 8:264. doi:10.4172/2157-7013. 1000264

Copyright: © 2017 Gai C, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Background: Adipose and bone marrow derived mesenchymal stem cells are two populations of multipotent adult stem cells with immunosuppressive, anti-inflammatory, and regenerative properties. It has been previously described that extracellular vesicles (EVs) derived from stem cells possess pro-regenerative and pro-angiogenic abilities. Hyperglycemia is a pathological condition affecting diabetic patients. Long term effects of hyperglycemia are endothelial dysfunction and vascular lesions leading to diabetic microangiopathy. The aim of the present study was to evaluate whether stem cell-derived EVs may inhibit endothelial cells dysfunction induced by hyperglycemia to mimic human microangiopathy.

Methods: We set up an in vitro hyperglycemic model by culturing human microvascular endothelial cells in hyperglycemic constant or intermittent conditions for 7 days, in order to mimic a chronic damage. At day 5, endothelial cells were incubated with adipose and mesenchymal stem cell-derived EVs or vehicle alone for 48 hr. At day 7, we evaluated apoptosis, oxidative stress, and capillary-like formation ability on Matrigel.

Results: Intermittent and constant high glucose models significantly decreased endothelial cell proliferation, increased number of apoptotic cells, promoted oxidation of intercellular proteins, and reduced capillary-like structure formation. Treatment with both kinds of EVs significantly restored proliferation, inhibited apoptosis and oxidation, and restored capillary-like formation.

Conclusions: The results of the present study demonstrate that adipose and bone marrow mesenchymal stem cell-derived EVs may inhibit the endothelial dysfunction induced by high glucose concentration, which mimic diabetic microvascular injury.


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