Abstract:
:An effective response to extreme hematopoietic stress requires an extreme elevation in hematopoiesis and preservation of hematopoietic stem cells (HSCs). These diametrically opposed processes are likely to be regulated by genes that mediate cellular adaptation to physiologic stress. Herein, we show that heme oxygenase-1 (HO-1), the inducible isozyme of heme degradation, is a key regulator of these processes. Mice lacking one allele of HO-1 (HO-1(+/-)) showed accelerated hematopoietic recovery from myelotoxic injury, and HO-1(+/-) HSCs repopulated lethally irradiated recipients with more rapid kinetics. However, HO-1(+/-) HSCs were ineffective in radioprotection and serial repopulation of myeloablated recipients. Perturbations in key stem cell regulators were observed in HO-1(+/-) HSCs and hematopoietic progenitors (HPCs), which may explain the disrupted response of HO-1(+/-) HPCs and HPCs to acute stress. Control of stem cell stress response by HO-1 presents opportunities for metabolic manipulation of stem cell-based therapies.
journal_name
Bloodjournal_title
Bloodauthors
Cao YA,Wagers AJ,Karsunky H,Zhao H,Reeves R,Wong RJ,Stevenson DK,Weissman IL,Contag CHdoi
10.1182/blood-2007-12-127621subject
Has Abstractpub_date
2008-12-01 00:00:00pages
4494-502issue
12eissn
0006-4971issn
1528-0020pii
blood-2007-12-127621journal_volume
112pub_type
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