| First Author | Hatazawa Y | Year | 2016 |
| Journal | Biochem Biophys Res Commun | Volume | 481 |
| Issue | 3-4 | Pages | 251-258 |
| PubMed ID | 27816452 | Mgi Jnum | J:240982 |
| Mgi Id | MGI:5896901 | Doi | 10.1016/j.bbrc.2016.10.133 |
| Citation | Hatazawa Y, et al. (2016) Deletion of the transcriptional coactivator PGC1alpha in skeletal muscles is associated with reduced expression of genes related to oxidative muscle function. Biochem Biophys Res Commun 481(3-4):251-258 |
| abstractText | The expression of the transcriptional coactivator PGC1alpha is increased in skeletal muscles during exercise. Previously, we showed that increased PGC1alpha leads to prolonged exercise performance (the duration for which running can be continued) and, at the same time, increases the expression of branched-chain amino acid (BCAA) metabolism-related enzymes and genes that are involved in supplying substrates for the TCA cycle. We recently created mice with PGC1alpha knockout specifically in the skeletal muscles (PGC1alpha KO mice), which show decreased mitochondrial content. In this study, global gene expression (microarray) analysis was performed in the skeletal muscles of PGC1alpha KO mice compared with that of wild-type control mice. As a result, decreased expression of genes involved in the TCA cycle, oxidative phosphorylation, and BCAA metabolism were observed. Compared with previously obtained microarray data on PGC1alpha-overexpressing transgenic mice, each gene showed the completely opposite direction of expression change. Bioinformatic analysis of the promoter region of genes with decreased expression in PGC1alpha KO mice predicted the involvement of several transcription factors, including a nuclear receptor, ERR, in their regulation. As PGC1alpha KO microarray data in this study show opposing findings to the PGC1alpha transgenic data, a loss-of-function experiment, as well as a gain-of-function experiment, revealed PGC1alpha's function in the oxidative energy metabolism of skeletal muscles. |
