FGF-2 inhibits TNF-α mediated apoptosis through upregulation of Bcl2-A1 and Bcl-xL in ATDC5 cells
Autor: | Yong-Min Kim, Youn-Moo Heo, Hak-Kyo Lee, Eung-Gook Kim, Sung Hoon Kim, Kwang-Yeol Lee, Joong-Kook Choi, Kyoung-Il Jeong, Seung-Ryul Kim, Hae Lan Jang, Chang Yeol Yeo, Hey-Ryun Kim |
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Rok vydání: | 2012 |
Předmět: |
Angiogenesis
Drug Evaluation Preclinical bcl-X Protein FGF-2 Down-Regulation Gene Expression Bcl-xL Apoptosis Fibroblast growth factor Biochemistry lcsh:Biochemistry Minor Histocompatibility Antigens chemistry.chemical_compound Mice Chondrocytes Pyrrolidine dithiocarbamate Animals lcsh:QD415-436 Molecular Biology lcsh:QH301-705.5 PI3K/AKT/mTOR pathway Cells Cultured Cell Proliferation biology Dose-Response Relationship Drug Kinase Chemistry Tumor Necrosis Factor-alpha Stem Cells General Medicine Bcl2-A1 Cell biology ATDC5 cells Up-Regulation lcsh:Biology (General) Proto-Oncogene Proteins c-bcl-2 TNF-α Immunology biology.protein Tumor necrosis factor alpha Fibroblast Growth Factor 2 |
Zdroj: | BMB Reports, Vol 45, Iss 5, Pp 287-292 (2012) |
ISSN: | 1976-670X |
Popis: | FGF-2 is involved in cell survival, proliferation, apoptosis, andangiogenesis in a wide variety of cells. FRGRs, PI3K and MAPkinases are well known mediators of FGF signaling. Despite itsknown roles during many developmental processes, includingosteogenesis, there are few known targets of FGF-2. In thepresent study, we identified Bcl2-A1 and Bcl-xL as two prominenttargets involved in promoting cell survival. Pretreatmentof ATDC5 cells with FGF-2 increased cell survival, whilesiRNAs specific for Bcl2-A1 and Bcl-xL compromised the anti-apoptotic effect of FGF-2, sensitized the cells to apoptosistriggered by TNF-α. Chemical inhibition of FGFR, NFkB, andPI3K activity by PD173074, pyrrolidine dithiocarbamate, andLY294002 respectively abrogated the FGF-2-mediated inductionof Bcl2-A1 and Bcl-xL expression. Taken together, our datademonstrate that a subset of Bcl2 family proteins are the targetsof FGF-2 signaling that promotes the survival of ATDC5cells. [BMB reports 2012; 45(5): 287-292] |
Databáze: | OpenAIRE |
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