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Prepublished online as a Blood First Edition Paper on October 3, 2002; DOI 10.1182/blood-2002-05-1505. This Article Full Text (PDF) All Versions of this Article: 2002-05-1505v1 101/3/1164    most recent Alert me when this article is cited Alert me if a correction is posted 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 Hasegawa, T. Articles by Kitagawa, S. Search for Related Content PubMed PubMed Citation Articles by Hasegawa, T. Articles by Kitagawa, S. Social Bookmarking                   What's this? Submitted May 23, 2002 Accepted September 4, 2002 Expression of the inhibitor of apoptosis (IAP) family members in human neutrophils: up-regulation of cIAP2 by granulocyte colony-stimulating factor and overexpression of cIAP2 in chronic neutrophilic leukemia Taro Hasegawa, Kenichi Suzuki, Chikahiko Sakamoto, Kensuke Ohta, Saori Nishiki, Masayuki Hino, Noriyuki Tatsumi, and Seiichi Kitagawa* Departments of Physiology and Clinical Hematology, Osaka City University Medical School, Osaka, Japan * Corresponding author; email: kitagawas{at}med.osaka-cu.ac.jp. Human neutrophils were found to express members of the inhibitor of apoptosis (IAP) family, namely cellular IAP1 (cIAP1), cIAP2 and X-linked IAP. Among these members, cIAP2 expression was selectively up-regulated by stimulation with granulocyte colony-stimulating factor (G-CSF), but not with granulocyte-macrophage CSF. The increased expression of cIAP2 mRNA was detected as early as 30 minutes after in vitro stimulation with G-CSF, and the elevated level of cIAP2 protein was detected at 1 hour. The elevated level of cIAP2 protein was also detected in peripheral blood neutrophils obtained from healthy donors receiving G-CSF administration. G-CSF-induced up-regulation of cIAP2 mRNA and protein, phosphorylation of signal transducer and activator of transcription 3 (STAT3), and anti-apoptotic effect were inhibited by pretreatment of cells with AG490, a specific inhibitor of Janus kinase 2 (JAK2). Mature neutrophils from a patient with chronic neutrophilic leukemia exhibited remarkable overexpression of cIAP2 mRNA and prolongation of survival, whereas cIAP2 mRNA expression and survival in mature neutrophils from patients with chronic myelogenous leukemia were essentially similar to those in normal neutrophils. These findings suggest that cIAP2 expression is up-regulated by G-CSF through activation of the JAK2-STAT3 pathway, and increased expression of cIAP2 protein may contribute to G-CSF-mediated anti-apoptosis. In addition, overexpression of cIAP2 may be partly responsible for sustained neutrophilia at least in some cases of chronic neutrophilic leukemia. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: O. Ma, W.-W. Cai, L. Zender, T. Dayaram, J. Shen, A. J. Herron, S. W. Lowe, T.-K. Man, C. C. Lau, and L. A. Donehower MMP13, Birc2 (cIAP1), and Birc3 (cIAP2), Amplified on Chromosome 9, Collaborate with p53 Deficiency in Mouse Osteosarcoma Progression Cancer Res., March 15, 2009; 69(6): 2559 - 2567. [Abstract] [Full Text] [PDF] S. A. Didichenko, N. Spiegl, T. Brunner, and C. A. 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