Send to

Choose Destination
Cell Cycle. 2010 May 15;9(10):2008-17. Epub 2010 May 15.

Upregulation of nascent mitochondrial biogenesis in mouse hematopoietic stem cells parallels upregulation of CD34 and loss of pluripotency: a potential strategy for reducing oxidative risk in stem cells.

Author information

Department of Microbiology and Immunology, Indiana University School of Medicine; Indianapolis, IN, USA.


Oxidative damage by reactive oxygen species generated in mitochondria is a potential cause of stem-cell dysregulation. Little is known about how hematopoietic stem cells mitigate/lessen this risk in the face of upregulated mitochondrial biogenesis/function necessary for the energy needs of differentiation and progenitor expansion. Here we report that upregulation of mitochondrial mass in mouse hematopoietic stem cells is closely linked to the appearance of CD34 on their surface, a marker indicating loss of long-term repopulating ability. These mitochondria have low membrane potential initially, but become active before exiting the primitive LSK compartment. Steady-state hematopoiesis perturbed by global expression of SDF-1/CXCL12 transgene causes a shift in ratios of these mitochondrialy-distinct LSK populations. Based on known effects of SDF-1 and signaling by it's receptor, CXCR4, along with finding primitive progenitors with high mitochondrial mass but low activity, we suggest a model of asymmetric self-renewing stem cell division that could lessen stem cell exposure to oxidative damage.

Comment in

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Taylor & Francis Icon for PubMed Central
Loading ...
Support Center