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Blood, 6 August 2009, Vol. 114, No. 6, pp. 1186-1195. Prepublished online as a Blood First Edition Paper on May 28, 2009; DOI 10.1182/blood-2008-09-179788. This Article Full Text Full Text (PDF) Supplemental Table and Figures All Versions of this Article: blood-2008-09-179788v1 114/6/1186    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Google Scholar Articles by Suh, H. C. Articles by Keller, J. R. PubMed PubMed Citation Articles by Suh, H. C. Articles by Keller, J. R. Related Collections Hematopoiesis and Stem Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS AND STEM CELLS Cell-nonautonomous function of Id1 in the hematopoietic progenitor cell niche Hyung Chan Suh1, Ming Ji1, John Gooya1, Michael Lee1, Kimberly D. Klarmann1, and Jonathan R. Keller1 1 Basic Research Program, SAIC-Frederick Inc, Center For Cancer Research, National Cancer Institute-Frederick, MD Development of hematopoietic stem cells (HSCs) and their immediate progeny is maintained by the interaction with cells in the microenvironment. We found that hematopoiesis was dysregulated in Id1–/– mice. Although the frequency of HSCs in Id1–/– bone marrow was increased, their total numbers remained unchanged as the result of decreased bone marrow cellularity. In addition, the ability of Id1–/– HSCs to self-renew was normal, suggesting Id1 does not affect HSC function. Id1–/– progenitors showed increased cycling in vivo but not in vitro, suggesting cell nonautonomous mechanisms for the increased cycling. Id1–/– HSCs developed normally when transplanted into Id1+/+ mice, whereas the development of Id1+/+ HSCs was impaired in Id1–/– recipients undergoing transplantation and reproduced the hematologic features of Id1–/– mice, indicating that the Id1–/– microenvironment cannot support normal hematopoietic development. Id1–/– stromal cells showed altered production of cytokines in vitro, and cytokine levels were deregulated in vivo, which could account for the Id1–/– hematopoietic phenotypes. Thus, Id1 is required for regulating the hematopoietic progenitor cell niche but is dispensable for maintaining HSCs. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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