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Blood, 15 May 2007, Vol. 109, No. 10, pp. 4494-4502. Prepublished online as a Blood First Edition Paper on February 6, 2007; DOI 10.1182/blood-2006-04-016154. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2006-04-016154v1 109/10/4494    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 HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Perry, J. M. Articles by Paulson, R. F. Search for Related Content PubMed PubMed Citation Articles by Perry, J. M. Articles by Paulson, R. F. Related Collections Hematopoiesis and Stem Cells Red Cells Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  RED CELLS BMP4, SCF, and hypoxia cooperatively regulate the expansion of murine stress erythroid progenitors John M. Perry3, Omid F. Harandi4, and Robert F. Paulson1,4 1 Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park; 2 Center for Molecular Immunology and Infectious Disease, The Pennsylvania State University, University Park; 3 Huck Institutes of the Life Sciences Cell and Developmental Biology Option, The Pennsylvania State University, University Park; 4 Graduate Program in Genetics, The Pennsylvania State University, University Park The erythroid response to acute anemia relies on the rapid expansion in the spleen of a specialized population of erythroid progenitors termed stress BFU-E. This expansion requires BMP4/Madh5-dependent signaling in vivo; however, in vitro, BMP4 alone cannot recapitulate the expansion of stress BFU-E observed in vivo, which suggests that other signals are required. In this report we show that mutation of the Kit receptor results in a severe defect in the expansion of stress BFU-E, indicating a role for the Kit/SCF signaling pathway in stress erythropoiesis. In vitro analysis showed that BMP4 and SCF are necessary for the expansion of stress BFU-E, but only when spleen cells were cultured in BMP4 + SCF at low-oxygen concentrations did we recapitulate the expansion of stress BFU-E observed in vivo. Culturing spleen cells in BMP4, SCF under hypoxic conditions resulted in the preferential expansion of erythroid progenitors characterized by the expression of Kit, CD71, and TER119. This expression pattern is also seen in stress erythroid progenitors isolated from patients with sickle cell anemia and patients with ß-thalassemia. Taken together these data demonstrate that SCF and hypoxia synergize with BMP4 to promote the expansion and differentiation of stress BFU-E during the recovery from acute anemia. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. Tanno, P. Porayette, O. Sripichai, S.-J. Noh, C. Byrnes, A. Bhupatiraju, Y. T. Lee, J. B. Goodnough, O. Harandi, T. Ganz, et al. Identification of TWSG1 as a second novel erythroid regulator of hepcidin expression in murine and human cells Blood, July 2, 2009; 114(1): 181 - 186. [Abstract] [Full Text] [PDF] J. M. Perry, O. F. Harandi, P. Porayette, S. Hegde, A. K. Kannan, and R. F. Paulson Maintenance of the BMP4-dependent stress erythropoiesis pathway in the murine spleen requires hedgehog signaling Blood, January 22, 2009; 113(4): 911 - 918. [Abstract] [Full Text] [PDF] N. Danilova, K. M. Sakamoto, and S. Lin Ribosomal protein S19 deficiency in zebrafish leads to developmental abnormalities and defective erythropoiesis through activation of p53 protein family Blood, December 15, 2008; 112(13): 5228 - 5237. [Abstract] [Full Text] [PDF] A. Subramanian, S. Hegde, P. Porayette, M. Yon, P. Hankey, and R. F. Paulson Friend Virus Utilizes the BMP4-Dependent Stress Erythropoiesis Pathway To Induce Erythroleukemia J. Virol., January 1, 2008; 82(1): 382 - 393. [Abstract] [Full Text] [PDF]

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