J Howard
J Otis


Jonathan Howard1,2, Jeff Otis2. 1Georgia Highlands College, Rome, GA. 2Georgia State University, Atlanta, GA.

BACKGROUND: The vitamin D receptor (VDR) is implicated in a host of immune system functions and more recently in skeletal muscle growth. While studies have shown a concomitant increase in VDR expression during strength training, none have quantified the amount of time that a single event of muscle injury has on VDR expression levels. Here, we quantified VDR gene levels over 4 weeks following significant injury in an attempt to gain insight on potential immune response targets to improve muscle recovery. METHODS: Tibialis anterior muscles from male C57Bl/6 mice (n=4-5/group) were injected with a 2% barium chloride (BaCl2) solution to initiate degeneration and regeneration processes. Regenerating muscles were then harvested at 1, 5, 10, or 28 days post-injury and VDR gene expression was compared to uninjured, control muscles. Several markers of oxidant stress were also quantified (previously published). The significance of differences was measured using t-tests. RESULTS: There was a slight, but insignificant increase in VDR expression 1 day post-injury (2.96-fold change, p = 0.14). However, VDR expression spiked 5 days post-injury (48.1-fold change, p = 0.01) and remained significantly elevated at 10- and 28-days post-injury (19.5- and 20.9-fold change, respectively). Total protein oxidant stress was also evident at 10 days after injury (p< 0.05). Markers of inflammation including interleukin 1 beta (IL1β), tumor necrosis factor alpha (TNFα), and interleukin 6 (IL6) were elevated 5 days post injury (p$lt; 0.05). CONCLUSION: Skeletal muscle damage appears to cause a substantial increase in induction of VDR within 5 days of injury and continues to remain elevated 28 days post injury. This appears to indicate that muscle damage may have a long-lasting effect on VDR expression which may provide oxidative stress protection and help normalize muscle regrowth following skeletal muscle injury.

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