| First Author | Martínez-Moreno M | Year | 2007 |
| Journal | J Biol Chem | Volume | 282 |
| Issue | 32 | Pages | 23044-54 |
| PubMed ID | 17519233 | Mgi Jnum | J:124608 |
| Mgi Id | MGI:3722026 | Doi | 10.1074/jbc.M610751200 |
| Citation | Martinez-Moreno M, et al. (2007) Nitric oxide down-regulates caveolin-3 levels through the interaction with myogenin, its transcription factor. J Biol Chem 282(32):23044-54 |
| abstractText | Certain patients suffering from chronic diseases such as AIDS or cancer experience a constant cellular secretion of tumor necrosis factor alpha and other pro-inflammatory cytokines that results in a continuous release of nitric oxide (*NO) to the bloodstream. One immediate consequence of the deleterious action of *NO is weight loss and the progressive destruction of muscular mass in a process known as cachexia. We have previously reported that caveolin-3, a specific marker of muscle cells, becomes down-regulated by the action of *NO on muscular myotubes. We describe herein that the changes observed in caveolin-3 levels are due to the alteration of the DNA binding activity of the muscular transcription factor myogenin. In the presence of *NO, the binding of transcription factors from cell nuclear extracts of muscular tissues to the E boxes present in the caveolin-3 promoter become substantially reduced. When we purified recombinant myogenin and treated it with *NO donors, we could detect its S-nitrosylation by three independent methods, suggesting that very likely one of the cysteine residues of the molecule is being modified. Given the role of myogenin as a regulatory protein that determines the level of multiple muscle genes expressed during late myogenesis, our results might represent a novel mode of regulation of muscle development under conditions of nitric oxide-mediated toxicity. |
