2010 Fiscal Year Final Research Report
The Biological role for Interferon regulatory fator 2
Project/Area Number |
20590081
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Biological pharmacy
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Research Institution | National Institute of Infectious Diseases |
Principal Investigator |
MASUMI Atsuko National Institute of Infectious Diseases, 血液・安全性研究部, 主任研究官 (70165728)
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Project Period (FY) |
2008 – 2010
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Keywords | インターフェロン制御転写因子 / 造血幹細胞 / 血液細胞分化 |
Research Abstract |
Megakaryopoiesis is associated with inflammation, and certain inflammatory cytokines stimulate hematopoietic progenitors to differentiate into megakaryocytes. Interferon-γ (IFN-γ) is an inflammatory cytokine that stimulates megakaryocyte development, and interferon regulatory factors (IRFs), IRF-1 and IRF-2 are typical transcription factors that are involved in IFN-γ response. We investigate the role of IRFs in megakaryopoiesis. To investigate the role of IRFs in megakaryopoiesis, mouse bone marrow hematopoietic stem cells (HSCs) were prepared and stimulated with IFN-γ. IFN-γ treatment induced IRF-2 expression as well as CD41 although their induction levels were much lower than that of IRF-1. When IRF expression levels were studied in mouse bone marrow cell fractions, IRF-2 expression was relatively high in HSCs. An in vitro clonogenic assay showed that IRF-2 overexpressed cells increased the number of megakaryocytic colonies, but not IRF-1 overexpressed cells, suggesting that IRF-2 is involved in megakaryopoiesis. Mechanistic analysis showed that IRF-2 transfection up-regulated CD41 promoter activity in hematopoietic cell lines through its binding to an ISRE-like site in the CD41 promoter. These findings suggest that IRF-2 plays an important role in megakaryocytic cell commitment or differentiation from hematopoietic stem cells by regulating CD41 expression in an inflammation state.
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[Journal Article] Enhanced RIG-I is mediated by interferon regulatory factor-2 in peripheral blood B cell from HCV-infected patients.2010
Author(s)
Masumi A., Ito M., Mochida K., Hamaguchi I., Mizukami T., Momose H., Kuramitsu M., Tsuruhara M., Kato A., Yamaguchi K.
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Journal Title
Biochem.Biophys.Res, Commun. 391
Pages: 1623-1628
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