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Blood, 1 November 2003, Vol. 102, No. 9, pp. 3154-3162. Prepublished online as a Blood First Edition Paper on July 10, 2003; DOI 10.1182/blood-2003-02-0367. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-02-0367v1 102/9/3154    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 Tanaka, M. Articles by Miyajima, A. Search for Related Content PubMed PubMed Citation Articles by Tanaka, M. Articles by Miyajima, A. Related Collections Hematopoiesis and Stem Cells Hemostasis, Thrombosis, and Vascular Biology Red Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS Targeted disruption of oncostatin M receptor results in altered hematopoiesis Minoru Tanaka, Yoko Hirabayashi, Takashi Sekiguchi, Tohru Inoue, Motoya Katsuki, and Atsushi Miyajima From the Institute of Molecular and Cellular Biosciences, University of Tokyo, Japan; Kanagawa Academy of Science and Technology, Kawasaki, Japan; National Institute of Health Sciences, Tokyo, Japan; and National Institute for Basic Biology, Okazaki National Research Institute, Okazaki, Japan. Oncostatin M (OSM) is a multifunctional cytokine that belongs to the interleukin 6 (IL-6) family. As OSM is expressed in adult as well as embryonic hematopoietic tissues, OSM has been considered to play a role in hematopoiesis. To uncover roles of OSM, we have generated mutant mice deficient in the OSM-specific receptor subunit (OSMR). While OSMR–/– mice were healthy and fertile, hematologic analysis of OSMR–/– mice demonstrated that the numbers of peripheral erythrocytes and platelets were reduced compared with wild-type mice. Consistent with this, progenitors of erythroid and megakaryocyte lineages were reduced in OSMR–/– bone marrow (BM), suggesting that OSM is required for the maintenance of erythroid and megakaryocyte progenitor pools in BM. To investigate whether OSM acts on the hematopoietic progenitors directly or indirectly, we performed BM transplantation experiments. The OSMR–/– mice, engrafted with wild-type BM cells, failed to produce erythrocytic and megakaryocytic progenitors to the levels in wild-type mice, indicating that OSM affects hematopoietic microenvironments. On the other hand, erythrocytic and megakaryocytic progenitors were reduced in the wild-type mice reconstituted with OSMR–/– BM cells. Thus, OSM regulates hematopoiesis in vivo by stimulating stromal cells as well as hematopoietic progenitors, in particular megakaryocytic and erythrocytic progenitors. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: P. J. Hohensinner, C. Kaun, K. Rychli, A. Niessner, S. Pfaffenberger, G. Rega, A. Furnkranz, P. Uhrin, J. Zaujec, T. Afonyushkin, et al. The inflammatory mediator oncostatin M induces stromal derived factor-1 in human adult cardiac cells FASEB J, March 1, 2009; 23(3): 774 - 782. [Abstract] [Full Text] [PDF] C. Hintzen, C. Evers, B. E. Lippok, R. Volkmer, P. C. Heinrich, S. Radtke, and H. M. Hermanns Box 2 Region of the Oncostatin M Receptor Determines Specificity for Recruitment of Janus Kinases and STAT5 Activation J. Biol. 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