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Publication : An embryonic CaVβ1 isoform promotes muscle mass maintenance via GDF5 signaling in adult mouse.

First Author  Traoré M Year  2019
Journal  Sci Transl Med Volume  11
Issue  517 PubMed ID  31694926
Mgi Jnum  J:294564 Mgi Id  MGI:6455375
Doi  10.1126/scitranslmed.aaw1131 Citation  Traore M, et al. (2019) An embryonic CaVbeta1 isoform promotes muscle mass maintenance via GDF5 signaling in adult mouse. Sci Transl Med 11(517)
abstractText  Deciphering the mechanisms that govern skeletal muscle plasticity is essential to understand its pathophysiological processes, including age-related sarcopenia. The voltage-gated calcium channel CaV1.1 has a central role in excitation-contraction coupling (ECC), raising the possibility that it may also initiate the adaptive response to changes during muscle activity. Here, we revealed the existence of a gene transcription switch of the CaV1.1 beta subunit (CaVbeta1) that is dependent on the innervation state of the muscle in mice. In a mouse model of sciatic denervation, we showed increased expression of an embryonic isoform of the subunit that we called CaVbeta1E. CaVbeta1E boosts downstream growth differentiation factor 5 (GDF5) signaling to counteract muscle loss after denervation in mice. We further reported that aged mouse muscle expressed lower quantity of CaVbeta1E compared with young muscle, displaying an altered GDF5-dependent response to denervation. Conversely, CaVbeta1E overexpression improved mass wasting in aging muscle in mice by increasing GDF5 expression. We also identified the human CaVbeta1E analogous and show a correlation between CaVbeta1E expression in human muscles and age-related muscle mass decline. These results suggest that strategies targeting CaVbeta1E or GDF5 might be effective in reducing muscle mass loss in aging.
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