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Journal of Tissue Science and Engineering

ISSN: 2157-7552

Open Access

Pot1a regulates self-renewal activity of hematopoietic stem cells


4th International Conference on Tissue Science and Regenerative Medicine

July 27-29, 2015 Rome, Italy

Fumio Arai

Scientific Tracks Abstracts: J Tissue Sci Eng

Abstract :

Aging or repeated cell division induces the accumulation of DNA damage which impairs hematopoietic stem cell (HSC) function. Protection of telomeres 1 (Pot1), a component of shelter in contributes to the suppression of unnecessary DNA damage response (DDR) at telomeres. We identified that high levels of Pot1a was expressed in HSCs and that this expression decreased shapely with age. Knockdown of Pot1a increased telomeric DDR and the frequency of symmetric differentiation divisions in cultures and significantly reduced long-term reconstitution (LTR) activity. In contrast, overexpression of Pot1a or treatment with exogenous Pot1a protein Pot1a protein prevented telomeric DDR and maintained symmetric self-renewing divisions and LTR activity in HSCs indicating that Pot1a rejuvenated stem cell activity of HSCs. Human POT1 protein also increased the number of cord blood HSCs. These data suggest that the protection of telomeric DNA from DDR signaling is critical for sustained selfrenewal of HSCs and that Pot1a is a novel target for ex vivo expansion of HSCs.

Biography :

Fumio Arai has completed his PhD from Meikai University and Postdoctoral studies from Keio University School of Medicine. He is a Professor of Department of stem cell biology and Medicine, Graduate School of Medical Sciences, Kyushu University. His research interest is in studying the mechanisms of the cell fate regulation of HSCs at the single cell level for the establishment of the system that is able to expand HSCs.

Information

Copyright: 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 work is properly cited.


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Received Date: Jan 01, 1970
Accepted Date: Jan 01, 1970
Published Date: Jan 01, 1970

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