Aging induced loss of stemness with concomitant gain of myogenic properties of a pure population of CD34(+)/CD45(-) muscle derived stem cells.

Autor: Bose B; School of Biological Sciences, Nanyang Technological University, 60, Nanyang Drive, Singapore 637551, Singapore. Electronic address: Bipasha.bose@yenepoya.edu.in., Shenoy PS; School of Biological Sciences, Nanyang Technological University, 60, Nanyang Drive, Singapore 637551, Singapore. Electronic address: shenoy2000@yahoo.com.
Jazyk: angličtina
Zdroj: The international journal of biochemistry & cell biology [Int J Biochem Cell Biol] 2016 Jan; Vol. 70, pp. 1-12. Date of Electronic Publication: 2015 Oct 13.
DOI: 10.1016/j.biocel.2015.10.009
Abstrakt: Aging is accompanied by the functional decline of cells, tissues, and organs, as well as, a striking increase in susceptibility to a wide range of diseases. Within a tissue, both differentiated cells and adult stem cells are susceptible to intrinsic and extrinsic changes while aging. Muscle derived stem cells (MDSCs) are tissue specific stem cells which have been studied well for their multipotential nature. Although there are reports relating to diminished function and regenerative capacity of aged MDSCs as compared to their young counterparts, not much has been reported relating to the concomitant gain in unipotent nature of aged MDSCs. In this study, we report an inverse correlation between aging and expression of adult/mesenchymal stem cell markers and a direct correlation between aging and myogenecity in MDSCs. Aged MDSCs were able to generate a greater number of dystrophin positive myofibres, as compared to, the young MDSCs when transplanted in muscle of dystrophic mice. Our data, therefore, suggests that aging stress adds to the decline in stem cell characteristics with a concomitant increase in unipotency, in terms of, myogenecity of MDSCs. This study, hence, also opens the possibilities of using unipotent aged MDSCs as potential candidates for transplantation in patients with muscular dystrophies.
(Copyright © 2015. Published by Elsevier Ltd.)
Databáze: MEDLINE
Externí odkaz: