2017 Volume 38 Pages 39-45
We have recently shown that heat stress 1) induces mitochondrial biogenesis, 2) improves mitochondrial dysfunction in denervated and aged muscles. However, its underlying mechanisms have been not understood. In this study, we tested our hypothesis that heat stress activates transcription of mitochondrial-related genes in skeletal muscle.
ICR mice were involved in this study. Mice were exposed into a hot environmental chamber (40ºC, 30 min). Immediately after treatment or three-hour after treatment, gastrocnemius muscles were collected. We performed several biochemical experiments such as real-time PCR and western blotting.
[Results and Discussion]
We found that heat stress increases mitochondrial genes encoded by both nDNA and mtDNA three-hour after heat stress treatment. We further examined next hypothesis that heat stress will activate tumor suppressor gene p53, which would contribute to increased expressions of mitochondrial-related genes. Unexpectedly, we did not observe data supporting p53 activation, based on no detectable changes in phosphorylated p53 and translocations of p53 proteins into nuclear and mitochondria from cytosol.
We here provide evidences that heat stress increases mitochondrial-related genes in skeletal muscle. We also found that p53 would not contribute to mitochondrial transcriptional activations.