271
Views
24
CrossRef citations to date
0
Altmetric
DNA DAMAGE RESPONSE IN CD133+ CELLS FROM UMBILICAL CORD BLOOD

DNA damage response in CD133 + stem/progenitor cells from umbilical cord blood: Low level of endogenous foci and high recruitment of 53BP1

, , &
Pages 301-309 | Received 11 Jan 2012, Accepted 23 Nov 2012, Published online: 08 Jan 2013
 

Abstract

Purpose: Human hematopoietic stem cells (HSC) are thought to be a major target of radiation-induced leukemogenesis and also provide a relevant cellular model for assessing cancer risk. Cluster of designation 133+ (CD133+) is a marker found in human progenitor and hematopoietic stem cells. Our study examined the repair of radiation-induced DNA double-strand breaks (DSB) in CD133 + umbilical cord blood cells (UCBC).

Materials and methods: After γ-irradiation, endogenous and induced DSB were evaluated in CD133 + UCBC, CD133 − UCBC and peripheral blood lymphocytes (PBL) in terms of phosphorylated histone 2A family member X (γH2AX) and tumor suppressor p53 binding protein 1 (53BP1) foci.

Results: We found that repair signaling in CD133 + UCBC is different from CD133 − UCBC and PBL. These differences include lower endogenous DSB levels and higher 53BP1 recruitment.

Conclusions: Our data, together with a recent report on radiation-induced γH2AX and 53BP1 foci in CD34 + cells, indicate enhanced DNA repair capacity in HSC as compared to mature lymphocytes.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.