| First Author | Buitrago C | Year | 2013 |
| Journal | J Steroid Biochem Mol Biol | Volume | 136 |
| Pages | 125-30 | PubMed ID | 23470620 |
| Mgi Jnum | J:198985 | Mgi Id | MGI:5499974 |
| Doi | 10.1016/j.jsbmb.2013.02.013 | Citation | Buitrago C, et al. (2013) Role of VDR in 1alpha,25-dihydroxyvitamin D3-dependent non-genomic activation of MAPKs, Src and Akt in skeletal muscle cells. J Steroid Biochem Mol Biol 136:125-30 |
| abstractText | 1alpha,25-dihydroxyvitamin D3 [1,25D] is recognized as a steroid hormone that rapidly elicits intracellular signals in various tissues. In skeletal myoblasts, we have previously demonstrated that one of the 1,25D-induced non-genomic effects is the upstream stimulation of MAPKs through Src activation. In this work, the data obtained suggest that the classical receptor of vitamin D (VDR) participates in non-transcriptional actions of 1,25D. We significantly reduced VDR expression by infection of C2C12 murine myoblasts with lentiviral particles containing the pLKO.1 plasmid with information to express a shRNA against mouse VDR. In these cells (C2C12-shVDR), Western blot analyses show that 1,25D-induced p38 MAPK activation and Src tyr416 phosphorylation were abolished. In addition, 1,25D-dependent activity of ERK1/2 was diminished in cells lacking VDR but to a lesser extent ( approximately -60%). Phosphorylation of Akt by 1,25D, recently demonstrated in C2C12 cells, in the present work also appeared to be partially dependent on VDR expression ( approximately 50% in C2C12-shVDR cells). Our results indicate that VDR is involved in 1,25D-induced rapid events related to survival/proliferation responses in skeletal muscle cells, providing relevant information on the mechanism of initiation of the non-genomic hormone signal. The participation of a VDR-independent non-genomic mechanism of action should also be taken into consideration. This article is part of a Special Issue entitled 'Vitamin D Workshop'. |
