scholarly journals Acute bout of resistance exercise increases vitamin D receptor protein expression in rat skeletal muscle

2015 ◽  
Vol 100 (10) ◽  
pp. 1168-1176 ◽  
Author(s):  
Yuhei Makanae ◽  
Riki Ogasawara ◽  
Koji Sato ◽  
Yusuke Takamura ◽  
Kenji Matsutani ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Vitamin D ◽  
Protein Expression ◽  
Resistance Exercise ◽  
Vitamin D Receptor ◽  
Receptor Protein ◽  
Rat Skeletal Muscle ◽  
Acute Bout

scholarly journals Vitamin D receptor protein is associated with interleukin-6 in human skeletal muscle

Endocrine ◽  
2014 ◽  
Vol 49 (2) ◽  
pp. 512-520 ◽  
Author(s):  
Rachele M. Pojednic ◽  
Lisa Ceglia ◽  
Alice H. Lichtenstein ◽  
Bess Dawson-Hughes ◽  
Roger A. Fielding
Keyword(s):  
Skeletal Muscle ◽  
Vitamin D ◽  
Vitamin D Receptor ◽  
Interleukin 6 ◽  
Human Skeletal Muscle ◽  
Receptor Protein

Effects of high-intensity intermittent swimming on PGC-1alpha protein expression in rat skeletal muscle

2005 ◽  
Vol 184 (1) ◽  
pp. 59-65 ◽  
Author(s):  
S. Terada ◽  
K. Kawanaka ◽  
M. Goto ◽  
T. Shimokawa ◽  
I. Tabata
Keyword(s):  
Skeletal Muscle ◽  
Protein Expression ◽  
High Intensity ◽  
Rat Skeletal Muscle

scholarly journals The vitamin D receptor regulates mitochondrial function in C2C12 myoblasts

2020 ◽  
Vol 318 (3) ◽  
pp. C536-C541 ◽  
Author(s):  
Stephen P. Ashcroft ◽  
Joseph J. Bass ◽  
Abid A. Kazi ◽  
Philip J. Atherton ◽  
Andrew Philp
Keyword(s):  
Skeletal Muscle ◽  
Vitamin D ◽  
Protein Content ◽  
Vitamin D Receptor ◽  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Oxidative Capacity ◽  
C2c12 Myoblasts

Vitamin D deficiency has been linked to a reduction in skeletal muscle function and oxidative capacity; however, the mechanistic bases of these impairments are poorly understood. The biological actions of vitamin D are carried out via the binding of 1α,25-dihydroxyvitamin D3 (1α,25(OH)2D3) to the vitamin D receptor (VDR). Recent evidence has linked 1α,25(OH)2D3 to the regulation of skeletal muscle mitochondrial function in vitro; however, little is known with regard to the role of the VDR in this process. To examine the regulatory role of the VDR in skeletal muscle mitochondrial function, we used lentivirus-mediated shRNA silencing of the VDR in C2C12 myoblasts (VDR-KD) and examined mitochondrial respiration and protein content compared with an shRNA scrambled control. VDR protein content was reduced by ~95% in myoblasts and myotubes ( P < 0.001). VDR-KD myoblasts displayed a 30%, 30%, and 36% reduction in basal, coupled, and maximal respiration, respectively ( P < 0.05). This phenotype was maintained in VDR-KD myotubes, displaying a 34%, 33%, and 48% reduction in basal, coupled, and maximal respiration ( P < 0.05). Furthermore, ATP production derived from oxidative phosphorylation (ATPOx) was reduced by 20%, suggesting intrinsic impairments within the mitochondria following VDR-KD. However, despite the observed functional decrements, mitochondrial protein content, as well as markers of mitochondrial fission were unchanged. In summary, we highlight a direct role for the VDR in regulating skeletal muscle mitochondrial respiration in vitro, providing a potential mechanism as to how vitamin D deficiency might impact upon skeletal muscle oxidative capacity.

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