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Altered Ca 2+ homeostasis in the skeletal muscle of DJ − 1 null mice

Altered Ca 2+ homeostasis in the skeletal muscle of DJ − 1 null mice,10.1016/j.neurobiolaging.2009.07.010,Neurobiology of Aging,Alexander Shtifman,Nan

Altered Ca 2+ homeostasis in the skeletal muscle of DJ − 1 null mice   (Citations: 1)
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Loss-of-function mutations in DJ−1 are associated with early-onset of Parkinson's disease. Although DJ−1 is ubiquitously expressed, the functional pathways affected by it remain unresolved. Here we demonstrate an involvement of DJ−1 in the regulation of Ca2+ homeostasis in mouse skeletal muscle. Using enzymatically dissociated flexor digitorum brevis muscle fibers from wild-type (wt) and DJ−1 null mice, we examined the effects of DJ−1 protein on resting, cytoplasmic [Ca2+] ([Ca2+]i) and depolarization-evoked Ca2+ release in the mouse skeletal muscle. The loss of DJ−1 resulted in a more than two-fold increase in resting [Ca2+]i. While there was no alteration in the resting membrane potential, there was a significant decrease in depolarization-evoked Ca2+ release from the sarcoplasmic reticulum in the DJ−1 null muscle cells. Consistent with the role of DJ−1 in oxidative stress regulation and mitochondrial functional maintenance, treatments of DJ−1 null muscle cells with resveratrol, a mitochondrial activator, or glutathione, a potent antioxidant, reversed the effects of the loss of DJ−1 on Ca2+ homeostasis. These results provide evidence of DJ−1's association with Ca2+ regulatory pathways in mouse skeletal muscle, and suggest the potential benefit of resveratrol to functionally compensate for the loss of DJ−1.
Journal: Neurobiology of Aging - NEUROBIOL AGING , vol. 32, no. 1, pp. 125-132, 2011
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