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Related Collections Hematopoiesis and Stem Cells Apoptosis Cell Cycle Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 October 2002, Vol. 100, No. 7, pp. 2463-2471 HEMATOPOIESIS The antiapoptosis protein survivin is associated with cell cycle entry of normal cord blood CD34+ cells and modulates cell cycle and proliferation of mouse hematopoietic progenitor cells Seiji Fukuda, Richard G. Foster, Scott B. Porter, and Louis M. Pelus From the Department of Microbiology and Immunology and the Walther Oncology Center, Indiana University School of Medicine; and the Walther Cancer Institute, Indianapolis, IN. The inhibitor of the apoptosis protein (IAP) survivin is expressed in proliferating cells such as fetal tissues and cancers. We previously reported that survivin is expressed and growth factor regulated in normal adult CD34+ cells. Herein, we examined survivin expression in CD34+ cells before and after cell cycle entry and demonstrate a role for survivin in cell cycle regulation and proliferation. Analysis of known human IAPs revealed that only survivin is cytokine regulated in CD34+ cells. Survivin expression is coincident with cell cycle progression. Up-regulation of survivin by thrombopoietin (Tpo), Flt3 ligand (FL), and stem cell factor (SCF) occurred in underphosphorylated-retinoblastoma protein (Rb)positive, Ki-67negative, and cyclin Dnegative CD34+ cells. Quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) and multivariate flow cytometry demonstrated that Tpo, SCF, and FL increase survivin mRNA and protein in quiescent G0 CD34+ cells without increasing Ki-67 expression, indicating that cytokine-stimulated up-regulation of survivin in CD34+ cells occurs during G0, before cells enter G1. Selective inhibition of the PI3-kinase/AKT and mitogen-activated protein kinase (MAPKp42/44) pathways blocked survivin up-regulation by growth factors before arresting cell cycle. Retrovirus transduction of survivin-internal ribosome entry site-enhanced green fluorescent protein (survivin-IRES-EGFP) in primary mouse marrow cells increased granulocyte macrophage-colony-forming units (CFU-GM) by 1.7- to 6.2-fold and the proportion of CFU-GM in S phase, compared to vector control. An antisense survivin construct decreased total and S-phase CFU-GM. These studies provide further evidence that survivin up-regulation by growth factors is not a consequence of cell cycle progression and strongly suggest that survivin is an important early event for cell cycle entry by CD34+ cells. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Fukuda, P. Singh, A. Moh, M. 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Omata Helicobacter pylori Induces I{kappa}B Kinase {alpha} Nuclear Translocation and Chemokine Production in Gastric Epithelial Cells Infect. Immun., March 1, 2006; 74(3): 1452 - 1461. [Abstract] [Full Text] [PDF] J. T. Mao, M. C. Fishbein, B. Adams, M. D. Roth, L. Goodglick, L. Hong, M. Burdick, E. R. M. Strieter, C. Holmes, D. P. Tashkin, et al. Celecoxib Decreases Ki-67 Proliferative Index in Active Smokers Clin. Cancer Res., January 1, 2006; 12(1): 314 - 320. [Abstract] [Full Text] [PDF] K. Kawamura, J. Fukuda, Y. Shimizu, H. Kodama, and T. Tanaka Survivin Contributes to the Anti-Apoptotic Activities of Transforming Growth Factor alpha in Mouse Blastocysts Through Phosphatidylinositol 3'-Kinase Pathway Biol Reprod, December 1, 2005; 73(6): 1094 - 1101. [Abstract] [Full Text] [PDF] M. Kozak A second look at cellular mRNA sequences said to function as internal ribosome entry sites Nucleic Acids Res., November 28, 2005; 33(20): 6593 - 6602. [Abstract] [Full Text] [PDF] Z. Wang, J. 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