Vitamin D deficiency is associated with falls, muscle weakness, and sarcopenia. Vitamin D receptor (VDR) deletion in mice reduces their grip strength and endurance.
This project investigates the effects of myocyte-specific Vitamin D receptor deletion (mVDR) on muscle regeneration and function after injury.
Floxed VDR mice and human skeletal actin Cre-recombinase mice were bred to generate mVDR mice. The controls were floxed mice without Cre. Ten-month old males (n = 11-13/group) were injected with Notexin in their right tibialis anterior (TA) to induce myocyte death. Each mouse also had a control injection of saline into the Left TA.
mVDR mice had decreased grip strength (rmANOVA, p<0.01), but there were no significant differences in endurance-distance or voluntary wheel-running. At 28 days, the notexin-treated TA mass in mVDR was 25% lighter than their left-TA control (p=0.045) and 18% heavier than notexin-treated FC mice TA.
Histological analysis of mVDR notexin-treated muscles showed a high proportion of central nuclei, indicating ongoing myocyte regeneration. Two of the mVDR mice had very pronounced fibrosis in their R TA muscle, whereas none of the controls had increased fibrosis.
In summary, mVDR mice showed decreased grip strength but increased TA weight after a notexin-model of muscle injury and regeneration. Further histological assessment will be performed to investigate increased TA mass and muscle morphology.