Interferon-γ attenuates the survival activity of G-CSF through PI3K/Akt signaling pathway in mouse multipotent progenitor cells

摘要: Apoptosis plays an important role in the injury to stem and progenitor compartments associated with aberrant interferon-gamma (IFN-γ) aplastic anemia (AA), which is characterized by loss of cells; however, its molecular mechanism poorly understood. In this study, we have addressed apoptotic function IFN-γ against hematopoietic and/or progenitors. Although granulocyte colony-stimulating factor (G-CSF) augmented survival proliferative differentiating activity 32D cells, mouse multipotent these effects were abolished susceptible apoptosis IFN-γ. attenuated Akt phosphorylated G-CSF a dose- time-dependent manner. Wortmannin, specific inhibitor phosphatidylinositol 3-kinase (PI3K), enhanced inhibitory effect on collaboration IFN-γ, suggesting that might converge PI3K pathway. We examined expression Bcl-2-associated death (Bad), works downstream Akt. increased Bad protein reduced G-CSF. induced cells through caspase Taken together, results suggest could exert action progenitors interference PI3K/Akt signaling Our findings may contribute understanding decreased number characteristic AA.