Cellular and Molecular Biology



Anti-death strategies against oxidative stress in grafted mesenchymal stem cells

Woochul Chang1*, Byeong-Wook Song2*, Jae-Youn Moon3*, Min-Ji Cha4, Onju Ham5,6, Se-Yeon Lee5,6, Eunmi Choi7, Eunhyun Choi8 and Ki-Chul Hwang5,7,8

1Department of Biology Education, Pusan National University, Busan, Republic of Korea, 2Institute of Catholic Integrative Medicine, Incheon St. Mary’s Hospital, The Catholic University of Korea College of Medicine, Incheon, Republic of Korea, 3Department of Cardiology, CHA Bundang Medical Center, CHA University, Sungnam, Republic of Korea, 4Deparment of Pathology and Inmunology, Washington University College of Medicine, St. Louis, USA, 5Cardiovascular Research Institute, Yonsei University College of Medicine, Seoul, Republic of Korea, 6Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Republic of Korea, 7Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Republic of Korea and 8Severance Integrative Research Institute for Cerebral & Cardiovascular Disease, Yonsei University Health System, Seoul, Republic of Korea
*These authors have contributed equally to this work.

Offprint requests to: Ki-Chul Hwang, Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea. e-mail: kchwang@yuhs.ac

Summary. Mesenchymal stem cells (MSCs) possess the potential for use in cell-based therapy for repair of myocardial injury. The therapeutic potential of MSCs is based on the capacity of MSCs to differentiate into cardiac tissue and release paracrine factors. However, a major problem in the clinical application of MSC-based therapy is the poor viability of transplanted MSCs at the site of graft due to harsh microenvironment conditions, such as ischemia and/or anoikis. Ischemia after myocardial infarction (MI) and interaction of MSCs with their niche is associated with increased production of reactive oxygen species (ROS). ROS hinder cell adhesion and induce detachment of cells, which induces anoikis signals in implanted MSCs. Therefore, strategies to regulate oxidative stress following the implantation of MSCs are therapeutically attractive. In this review, we first describe ROS as a major obstacle in MSC-based therapy and focus on manipulation of implanted MSCs to reduce ROS-mediated anoikis
. Histol Histopathol 28, 1529-1536 (2013)

Key words: Mesenchymal stem cells, Reactive oxygen species, Anoikis, Myocardial infarction

DOI: 10.14670/HH-28.1529