NOS isoform-specific regulation of basal but not exercise-induced mitochondrial biogenesis in mouse skeletal muscle

G D Wadley, Julia Choate, Glenn K McConell

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Nitric oxide is a potential regulator of mitochondrial biogenesis. Therefore, we investigated if mice deficient in endothelial nitric oxide synthase (eNOS(-/-)) or neuronal NOS (nNOS(-/-)) have attenuated activation of skeletal muscle mitochondrial biogenesis in response to exercise. eNOS(-/-), nNOS(-/-) and C57Bl/6 (CON) mice (16.3 +/- 0.2 weeks old) either remained in their cages (basal) or ran on a treadmill (16 m.min(-1), 5 grade) for 60 min (n=8 per group) and were killed six hours after exercise. Other eNOS(-/-), nNOS(-/-) and CON mice exercise trained for 9 days (60 and were killed 24 hr after the last bout of exercise training. eNOS(-/-) mice had significantly higher nNOS protein and nNOS(-/-) mice had significantly higher eNOS protein in the EDL, but not the soleus. Basal mitochondrial biogenesis markers: NRF1, NRF2alpha and mtTFA mRNA were significantly (P
Original languageEnglish
Pages (from-to)253 - 262
Number of pages10
JournalThe Journal of Physiology
Issue numberPt 1
Publication statusPublished - 2007

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