Blood online
Home About Blood Authors Subscriptions Permission Advertising Public Access contact us
 

 
Advanced
Current Issue
First Edition
Future Articles
Archives
Submit to Blood
Search
American Society of Hematology
Meeting Abstracts
Email Alerts
 Blood, 1 December 2008, Vol. 112, No. 12, pp. 4494-4502.
Prepublished online as a Blood First Edition Paper on May 28, 2008; DOI 10.1182/blood-2007-12-127621.

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental Figures
Right arrow All Versions of this Article:
blood-2007-12-127621v1
112/12/4494    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Right arrow Rights and Permissions
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cao, Y.-A.
Right arrow Articles by Contag, C. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cao, Y.-A.
Right arrow Articles by Contag, C. H.
Related Collections
Right arrow Hematopoiesis and Stem Cells
Right arrowRelated Article in Blood Online
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

arrow to previous article Previous Article  |  Table of Contents  |  Next Article next article arrow

HEMATOPOIESIS AND STEM CELLS

Heme oxygenase-1 deficiency leads to disrupted response to acute stress in stem cells and progenitors

Yu-An Cao1, Amy J. Wagers2, Holger Karsunky2, Hui Zhao1, Robert Reeves1, Ronald J. Wong1, David K. Stevenson1, Irving L. Weissman2, and Christopher H. Contag1,3

1 Departments of Pediatrics, 2 Pathology, and 3 Radiology and Microbiology & Immunology, Stanford University School of Medicine, CA

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.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?

Related Article in Blood Online:

HO-1 extends to stem cells
Richard J. Cornall
Blood 2008 112: 4363-4364. [Full Text] [PDF]





click for free articles
home about blood authors subscriptions permissions advertising public access contact us
  Copyright © 2008 by American Society of Hematology         Online ISSN: 1528-0020