ArticleCell death & disease2016
Functional KCa1.1 channels are crucial for regulating the proliferation, migration and differentiation of human primary skeletal myoblasts.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 21 citations in OpenAlex.
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- Skeletal muscle gene expression dysregulation in long-term spaceflights and aging is clock-dependent.NPJ microgravity · 2023Article
- Muscle Damage in Dystrophic mdx Mice Is Influenced by the Activity of CaLife (Basel, Switzerland) · 2022Article
- Transcriptomic characterization of the molecular mechanisms induced by RGMa during skeletal muscle nuclei accretion and hypertrophy.BMC genomics · 2022Article
- Ion Channels and Transporters in Muscle Cell Differentiation.International journal of molecular sciences · 2021Review
- Antioxidant Carbon Nanoparticles Inhibit Fibroblast-Like Synoviocyte Invasiveness and Reduce Disease Severity in a Rat Model of Rheumatoid Arthritis.Antioxidants (Basel, Switzerland) · 2020Article
- Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration.Frontiers in physiology · 2020Article
- Genome wide analysis of gene expression changes in skin from patients with type 2 diabetes.PloS one · 2020Article
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- Targeting KCa1.1 Channels with a Scorpion Venom Peptide for the Therapy of Rat Models of Rheumatoid Arthritis.The Journal of pharmacology and experimental therapeutics · 2018Article
- KCa1.1 channels regulate βFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Optimization of Xenografting Methods for Generating Human Skeletal Muscle in Mice.Cell transplantationArticle
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Myoblasts are mononucleated precursors of myofibers; they persist in mature skeletal muscles for growth and regeneration post injury. During myotonic dystrophy type 1 (DM1), a complex autosomal-dominant neuromuscular disease, the differentiation of skeletal myoblasts into functional myotubes is impaired, resulting in muscle wasting and weakness. The mechanisms leading to this altered differentiation are not fully understood. Here, we demonstrate that the calcium- and voltage-dependent potassium channel, KCa1.1 (BK, Slo1, KCNMA1), regulates myoblast proliferation, migration, and fusion. We also show a loss of plasma membrane expression of the pore-forming α subunit of KCa1.1 in DM1 myoblasts. Inhibiting the function of KCa1.1 in healthy myoblasts induced an increase in cytosolic calcium levels and altered nuclear factor kappa B (NFκB) levels without affecting cell survival. In these normal cells, KCa1.1 block resulted in enhanced proliferation and decreased matrix metalloproteinase secretion, migration, and myotube fusion, phenotypes all observed in DM1 myoblasts and associated with disease pathogenesis. In contrast, introducing functional KCa1.1 α-subunits into DM1 myoblasts normalized their proliferation and rescued expression of the late myogenic marker Mef2. Our results identify KCa1.1 channels as crucial regulators of skeletal myogenesis and suggest these channels as novel therapeutic targets in DM1.
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