| Prostaglandin F2alpha promotes muscle cell survival and growth through upregulation of the inhibitor of apoptosis protein BRUCE. | |
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MedLine Citation:
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PMID: 18566603 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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During skeletal muscle growth and regeneration, the majority of differentiating myoblasts undergoes cell-cell fusion to form multinucleated myofibers, whereas a proportion of myoblasts undergoes apoptosis. The treatment of myoblasts with prostaglandin F2alpha (PGF2alpha) during myogenesis in vitro leads to the formation of large myotubes, but the mechanism by which PGF2alpha promotes myotube growth has not been investigated. Here, we demonstrate that PGF2alpha reduces cell death during myogenesis in vitro and in vivo. In addition, we show that PGF2alpha increases expression of the inhibitor of apoptosis protein (IAP) BRUCE through a pathway dependent on the nuclear factor of activated T cell 2 transcription factor. Importantly, PGF2alpha-mediated reduction in muscle cell death is dependent on BRUCE, and overexpression of BRUCE is sufficient to promote muscle cell survival and growth. These results establish a previously unrecognized link between NFAT signaling and regulation of IAP expression and are the first to identify a signaling pathway that increases BRUCE expression. In addition, our results provide evidence that increasing the pool of muscle cells available for fusion by inhibiting cell death enhances myotube growth. |
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Authors:
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K M Jansen; G K Pavlath |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2008-06-20 |
Journal Detail:
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Title: Cell death and differentiation Volume: 15 ISSN: 1350-9047 ISO Abbreviation: Cell Death Differ. Publication Date: 2008 Oct |
Date Detail:
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Created Date: 2008-09-16 Completed Date: 2008-10-27 Revised Date: 2010-08-09 |
Medline Journal Info:
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Nlm Unique ID: 9437445 Medline TA: Cell Death Differ Country: England |
Other Details:
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Languages: eng Pagination: 1619-28 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, Emory University School of Medicine, Emory University, Atlanta, GA 30322, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / physiology* Cell Survival / physiology* Cell Transplantation Cells, Cultured Dinoprost / genetics, metabolism* Female Inhibitor of Apoptosis Proteins / genetics, metabolism* Mice Mice, Inbred BALB C Mice, Knockout Microarray Analysis Muscle Development / physiology Muscle, Skeletal / cytology*, physiology Myoblasts / cytology, physiology* NFATC Transcription Factors / genetics, metabolism Signal Transduction / physiology Up-Regulation |
| Grant Support | |
ID/Acronym/Agency:
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AR-047314/AR/NIAMS NIH HHS; AR-051372/AR/NIAMS NIH HHS; AR-052730/AR/NIAMS NIH HHS; R01 AR052730-01A1/AR/NIAMS NIH HHS; R01 AR052730-02/AR/NIAMS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/BIRC6 protein, mouse; 0/Inhibitor of Apoptosis Proteins; 0/NFATC Transcription Factors; 0/Nfatc1 protein, mouse; 551-11-1/Dinoprost |
| Comments/Corrections | |
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