| Caspase-dependent apoptosis and -independent poly(ADP-ribose) polymerase cleavage induced by transforming growth factor beta1. | |
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MedLine Citation:
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PMID: 14643888 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Apoptosis is an important cell suicide program which involves the caspases activation and is implicated in physiological and pathological processes. Poly(ADP-ribose) polymerase (PARP) cleavage is often associated with apoptosis and has been served as one hallmark of apoptosis and caspase activation. In this study, we aimed to determine TGF-beta1-induced apoptosis and to examine the involvement of caspases and its relationship with PARP cleavage. TGF-beta1 induces strong apoptosis of AML-12 cells which can be detected by DNA fragmentation, FACS, and morphological assays. Z-VAD-fmk, a selective caspase inhibitor, partially inhibits the TGF-beta1-induced apoptosis; but has no effect on TGF-beta1-induced DNA fragmentation and PARP cleavage. However, BD-fmk, a broad-spectrum caspase inhibitor, completely suppresses TGF-beta1-induced apoptosis, but unexpectedly does not inhibit TGF-beta1-induced PARP cleavage. Furthermore, Z-VAD-fmk treatment is able to completely inhibit the daunorubicin-induced apoptosis in A-431 cells, but only slightly blocks the daunorubicin-induced PARP cleavage, whereas BD-fmk can inhibit both daunorubicin-induced apoptosis and PARP cleavage completely. In addition, we observed that both TGF-beta1-induced apoptosis and PARP degradation in AML-12 cells can be completely blocked by inhibiting the protein synthesis with cycloheximide. These results demonstrate for the first time that TGF-beta1-induced caspase-dependent apoptosis is associated with caspase-independent PARP cleavage that requires the TGF-beta1-induced synthesis of new proteins. The results indicate that caspase-3 is not a major caspase involved in TGF-beta1-induced apoptosis in AML-12 cells, and is not required for apoptosis-associated DNA fragmentation. The results also suggest that PARP cleavage may occur as an independent event that can be disassociated with cell apoptosis. |
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Authors:
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Yanan Yang; Sheng Zhao; Jianguo Song |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: The international journal of biochemistry & cell biology Volume: 36 ISSN: 1357-2725 ISO Abbreviation: Int. J. Biochem. Cell Biol. Publication Date: 2004 Feb |
Date Detail:
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Created Date: 2003-12-03 Completed Date: 2004-08-05 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 9508482 Medline TA: Int J Biochem Cell Biol Country: England |
Other Details:
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Languages: eng Pagination: 223-34 Citation Subset: IM |
Affiliation:
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Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yue-Yang Road, 200031, Shanghai, China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Amino Acid Chloromethyl Ketones
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pharmacology Animals Apoptosis* Caspases / metabolism* Cell Line Cell Separation Cycloheximide / pharmacology DNA Fragmentation Daunorubicin / pharmacology Enzyme Inhibitors / pharmacology Flow Cytometry Hepatocytes / pathology Immunoblotting Mice Microscopy, Fluorescence Poly(ADP-ribose) Polymerases / metabolism* Protein Kinase C / metabolism Protein Kinase C-delta Protein Synthesis Inhibitors / pharmacology Time Factors Transforming Growth Factor beta / metabolism* Transforming Growth Factor beta1 |
| Chemical | |
Reg. No./Substance:
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0/Amino Acid Chloromethyl Ketones; 0/Enzyme Inhibitors; 0/Protein Synthesis Inhibitors; 0/Tgfb1 protein, mouse; 0/Transforming Growth Factor beta; 0/Transforming Growth Factor beta1; 0/benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; 20830-81-3/Daunorubicin; 66-81-9/Cycloheximide; EC 2.4.2.30/Poly(ADP-ribose) Polymerases; EC 2.7.1.-/Prkcd protein, mouse; EC 2.7.11.13/Protein Kinase C; EC 2.7.11.13/Protein Kinase C-delta; EC 3.4.22.-/Caspases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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