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Oxidative Medicine and Cellular Longevity
Volume 2015, Article ID 486263, 11 pages
http://dx.doi.org/10.1155/2015/486263
Review Article

Reactive Oxygen Species in Mesenchymal Stem Cell Aging: Implication to Lung Diseases

1Department of Thoracic and Cardiovascular Surgery, School of Medicine, Kangwon National University, Chuncheon 200-701, Republic of Korea
2Institute of Medical Science, Kangwon National University, Chuncheon 200-701, Republic of Korea
3Adult Stem Cell Research Center, College of Veterinary Medicine, Seoul National University, Seoul 151-742, Republic of Korea

Received 10 October 2014; Revised 15 April 2015; Accepted 1 May 2015

Academic Editor: Cristina Angeloni

Copyright © 2015 Se-Ran Yang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

MSCs have become an emerging cell source with their immune modulation, high proliferation rate, and differentiation potential; indeed, they have been challenged in clinical trials. Recently, it has shown that ROS play a dual role as both deleterious and beneficial species depending on their concentration in MSCs. Various environmental stresses-induced excessive production of ROS triggers cellular senescence and abnormal differentiation on MSCs. Moreover, MSCs have been suggested to participate in the treatment of ALI/ARDS and COPD as a major cause of high morbidity and mortality. Therapeutic mechanisms of MSCs in the treatment of ARDS/COPD were focused on cell engraftment and paracrine action. However, ROS-mediated therapeutic mechanisms of MSCs still remain largely unknown. Here, we review the key factors associated with cell cycle and chromatin remodeling to accelerate or delay the MSC aging process. In addition, the enhanced ROS production and its associated pathophysiological pathways will be discussed along with the MSC senescence process. Furthermore, the present review highlights how the excessive amount of ROS-mediated oxidative stress might interfere with homeostasis of lungs and residual lung cells in the pathogenesis of ALI/ARDS and COPD.