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Blood, 22 January 2009, Vol. 113, No. 4, pp. 911-918. Prepublished online as a Blood First Edition Paper on October 16, 2008; DOI 10.1182/blood-2008-03-147892. This Article Full Text Full Text (PDF) Supplemental Figure All Versions of this Article: blood-2008-03-147892v1 113/4/911    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 Red Cells, Iron, and Erythropoiesis Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  RED CELLS, IRON, AND ERYTHROPOIESIS Maintenance of the BMP4-dependent stress erythropoiesis pathway in the murine spleen requires hedgehog signaling John M. Perry1, Omid F. Harandi2, Prashanth Porayette3, Shailaja Hegde4,5, Arun K. Kannan4, and Robert F. Paulson15 1 Cell and Developmental Biology Option 2 Graduate Program in Genetics 3 Molecular Medicine Option 4 Department of Veterinary and Biomedical Sciences, Huck Institutes of the Life Sciences, and the 5 Center for Molecular Immunology and Infectious Disease, Pennsylvania State University, University Park The production of mature cells necessitates that lineage-committed progenitor cells be constantly generated from multipotential progenitors. In addition, the ability to respond rapidly to physiologic stresses requires that the signals that regulate the maintenance of progenitor populations be coordinated with the signals that promote differentiation of progenitors. Here we examine the signals that are necessary for the maintenance of the BMP4-dependent stress erythropoiesis pathway. Our previous work demonstrated that BMP4, stem cell factor, and hypoxia act in concert to promote the expansion of a specialized population of stress erythroid progenitors in the spleen during the recovery from acute anemia. Our analysis shows that acute anemia leads to an almost complete mobilization of BMP4-responsive stress erythroid burst-forming units; therefore, new stress progenitors must be recruited to the spleen to replenish this system. We show that bone marrow cells can home to the spleen and, in response to a signal in the spleen microenvironment, Hedgehog, they develop into BMP4-responsive stress progenitors. Hedgehog induces the expression of BMP4, and together these 2 signals are required for the development of BMP4-responsive stress progenitors. These data demonstrate that the interplay between these 2 signals is crucial for maintenance of this stress response pathway. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: W.-K. Kim, V. Meliton, K. W. Park, C. Hong, P. Tontonoz, P. Niewiadomski, J. A. Waschek, S. Tetradis, and F. Parhami Negative Regulation of Hedgehog Signaling by Liver X Receptors Mol. Endocrinol., October 1, 2009; 23(10): 1532 - 1543. [Abstract] [Full Text] [PDF] A. R. Migliaccio, F. Martelli, M. Verrucci, M. Sanchez, M. Valeri, G. Migliaccio, A. M. Vannucchi, M. Zingariello, A. Di Baldassarre, B. Ghinassi, et al. Gata1 expression driven by the alternative HS2 enhancer in the spleen rescues the hematopoietic failure induced by the hypomorphic Gata1low mutation Blood, September 3, 2009; 114(10): 2107 - 2120. [Abstract] [Full Text] [PDF]

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