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Transforming growth factor-β1 and bone morphogenetic protein-2 downregulate CaV3.1 channel expression in mouse C2C12 myoblasts

Authors

  • Traudy Avila,

    1. Department of Physiology, Biophysics and Neuroscience, Center for Research and Advanced Studies of the National Polytechnic Institute (Cinvestav-IPN), Mexico City, Mexico
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  • Arturo Andrade,

    1. Department of Physiology, Biophysics and Neuroscience, Center for Research and Advanced Studies of the National Polytechnic Institute (Cinvestav-IPN), Mexico City, Mexico
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  • Ricardo Felix

    Corresponding author
    1. Department of Cell Biology; Cinvestav-IPN, Mexico City, Mexico
    • Departamento de Biología Celular, Cinvestav-IPN, Avenida IPN #2508, Colonia Zacatenco, México D.F., CP 07300, México.
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Abstract

In the developing skeletal muscle, fusion of myoblasts and myotube formation is a process that involves Ca2+ influx through T-type (CaV3) channels. Treatment of myoblasts with transforming growth factor-β1 (TGF-β1) and bone morphogenetic protein-2 (BMP-2) decreases the number of CaV3 channels in the plasma membrane and reduces myotube formation. In the current report, we examined whether the inhibitory actions of TGF-β1 and BMP-2 involve alterations in CaV3 mRNA expression in the myoblast C2C12 cell line. Using RT-PCR, we found that CaV3.1 but not CaV3.2 and CaV3.3 transcripts are present in either undifferentiated or fusion competent C2C12 myoblasts. Semi-quantitative analysis revealed a significant decrease of CaV3.1 mRNA expression in cells treated with TGF-β1 and BMP-2. In contrast, patch-clamp recordings on HEK-293 cells stably expressing recombinant CaV3.1 channels showed that T-type currents were not affected by chronic exposure to the growth factors. These results suggest that muscle T-channel downregulation by TGF-β1 and BMP-2 may be mediated by reduced transcription rather than through post-transcriptional modifications of CaV3.1 channels. J. Cell. Physiol. 209: 448–456, 2006. © 2006 Wiley-Liss, Inc.

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