ArticleActa physiologica (Oxford, England)2018
Physiological role of Kvβ2 (AKR6) in murine skeletal muscle growth and regulation.
Article in Acta physiologica (Oxford, England), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Genetic deletion of Kvβ2 (AKR6) causes loss of muscle function and increased inflammation in mice.Frontiers in aging · 2023Article
- Nampt activator P7C3 ameliorates diabetes and improves skeletal muscle function modulating cell metabolism and lipid mediators.Journal of cachexia, sarcopenia and muscle · 2022Article
- Metabolic regulation of Kv channels and cardiac repolarization by Kvβ2 subunits.Journal of molecular and cellular cardiology · 2019Article
- Emerging roles for multifunctional ion channel auxiliary subunits in cancer.Cell calcium · 2019Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
aimPotassium channel accessory subunits (Kvβ) play a key role in cardiac electrical activity through ion channel modulation. In this study, we hypothesize that Kvβ2 regulates skeletal muscle growth and fibre phenotype via protein-protein interactions.
methodsKvβ2 knockout mouse model was used for morphometric, immunohistochemical and biochemical analysis to evaluate the role of Kvβ2 in skeletal muscle physiology.
resultsDeletion of Kvβ2 gene in mice (Kvβ2 knockout, KO) leads to significant decrease in body weight along with skeletal muscle size. Key hindlimb muscles such as biceps, soleus and gastrocnemius were significantly smaller in size in KO mice compared to that of wild type. Morphometric measurements and histological analysis clearly point that the fibre size is decreased in each of the muscle type in KO compared with wild-type mice. In addition, Kvβ2 deletion contributes to fibre-type switching from fast to slow fibre as indicated by more abundant MHCI-expressing fibres in gastrocnemius and soleus muscles, which may underscore the smaller muscle size alongside increase in U3 ubiquitin ligase; NEDD4 expression. Using targeted siRNA knockdown approach, we identified that Kvβ2 knockdown does not affect the myoblasts proliferation. However, Pax7 expression was significantly decreased in 4-week-old gastrocnemius muscle, suggesting that cellular reserve for growth may be deficient in KO mice. This is further supported by decreased migratory capacity of C2C12 cells upon siRNA-targeted Kvβ2 knockdown.
conclusionOverall, this is the first report identifying that genetic deletion of Kvβ2 leads to decreased skeletal muscle size along with isotype switching.
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