Journal home
Advance online publication
Current issue
Archive
Press releases
Supplements
Focuses
Guide to authors
Online submissionOnline submission
For referees
Free online issue
Contact the journal
Subscribe
Advertising
work@npg
Reprints and permissions
About this site
For librarians
 
NPG Resources
Nature
Nature Reviews
Nature Immunology
Nature Cell Biology
Nature Genetics
news@nature.com
Nature Conferences
Dissect Medicine
NPG Subject areas
Biotechnology
Cancer
Chemistry
Clinical Medicine
Dentistry
Development
Drug Discovery
Earth Sciences
Evolution & Ecology
Genetics
Immunology
Materials Science
Medical Research
Microbiology
Molecular Cell Biology
Neuroscience
Pharmacology
Physics
Browse all publications
Technical Report
Nature Medicine  9, 1428 - 1432 (2003)
Published online: 26 October 2003; | doi:10.1038/nm951

In vitro expansion of hematopoietic stem cells by recombinant TAT-HOXB4 protein

Jana Krosl1, 5, Pamela Austin1, 5, Nathalie Beslu1, 5, Evert Kroon1, 5, R Keith Humphries2 & Guy Sauvageau1, 3, 4, 5

1  Laboratory of Molecular Genetics of Hemopoietic Stem Cells, Clinical Research Institute of Montreal, Montreal, Quebec, Canada, H2W 1R7.

2  Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, British Columbia, Canada, V5Z 1L3.

3  Department of Medicine and Division of Hematology, Hospital Maisonneuve-Rosemont, Montreal, Quebec, Canada, H1T 2M4.

4  Montreal University, Montreal, Quebec, Canada, H3C 3J7.

5  Present address: Institute of Research in Immunology and Cancer, University of Montreal, CP 6128, Downtown Station, Montreal, Quebec, Canada, H3C 3J7.

Correspondence should be addressed to Guy Sauvageau guy.sauvageau@umontreal.ca
Hematopoietic stem cells (HSCs) can self-renew extensively after transplantation. The conditions supporting their in vitro expansion are still being defined. Retroviral overexpression of the human homeobox B4 (HOXB4) gene in mouse bone marrow cells enables over 40-fold expansion of HSCs in vitro. To circumvent the requirement for retroviral infection, we used recombinant human TAT-HOXB4 protein carrying the protein transduction domain of the HIV transactivating protein (TAT) as a potential growth factor for stem cells. HSCs exposed to TAT-HOXB4 for 4 d expanded by about four- to sixfold and were 8−20 times more numerous than HSCs in control cultures, indicating that HSC expansion induced by TAT-HOXB4 was comparable to that induced by the human HOXB4 retrovirus during a similar period of observation. Our results also show that TAT-HOXB4-expanded HSC populations retain their normal in vivo potential for differentiation and long-term repopulation. It is thus feasible to exploit recombinant HOXB4 protein for rapid and significant ex vivo expansion of normal HSCs.

MORE ARTICLES LIKE THIS
These links to content published by NPG are automatically generated

REFERENCE
Mammalian Embryo: Wnt Signalling
Nature Encyclopaedia of Life Sciences
 See all 2 matches for Reference

REVIEWS
Hematopoietic cytokines, transcription factors and lineage commitment
Oncogene Reviews (15 May 2002)
 See all 3 matches for Reviews

RESEARCH
A role for Wnt signalling in self-renewal of haematopoietic stem cells
Nature Article (22 May 2003)
Enforced expression of EBF in hematopoietic stem cells restricts lymphopoiesis to the B cell lineage
The EMBO Journal Article (15 Sep 2003)
Identification of the haematopoietic stem cell niche and control of the niche size
Nature Letters to Editor (23 Oct 2003)
 See all 10 matches for Research

 Top
Abstract
Previous
Table of contents
Full textFull text
Download PDFDownload PDF
Send to a friendSend to a friend
Figures & Tables
Export citation
natureproducts

Search buyers guide:

 
ADVERTISEMENT
 
Nature Medicine
ISSN: 1078-8956
EISSN: 1546-170X
Journal home | Advance online publication | Current issue | Archive | Press releases | Supplements | Focuses | For authors | Online submission | For referees | Free online issue | About the journal | Contact the journal | Subscribe | Advertising | work@npg | Reprints and permissions | About this site | For librarians
Nature Publishing Group, publisher of Nature, and other science journals and reference works©2003 Nature Publishing Group | Privacy policy