Dent 2019 J Appl Physiol (1985)
|Dent JR, Hetrick B, Tahvilian S, Sathe A, Greyslak K, LaBarge SA, Svensson K, McCurdy CE, Schenk S (2019) Skeletal muscle mitochondrial function and exercise capacity is not impaired in mice with knockout of STAT3. J Appl Physiol (1985) [Epub ahead of print].|
Abstract: Signal transducer and activator of transcription 3 (STAT3) was recently found to be localized to mitochondria in a number of tissues and cell types, where it modulates oxidative phosphorylation via interactions with the electron transport proteins, complex I and complex II. Skeletal muscle is densely populated with mitochondria, althoughwhether STAT3 contributes to skeletal muscle oxidative capacity is unknown. In the present study we sought to elucidate the contribution of STAT3 to mitochondrial and skeletal muscle function by studying mice with muscle-specific knockout of STAT3 (mKO). First, we developed a novel flow cytometry-based approach to confirm that STAT3 is present in skeletal muscle mitochondria. However, contrary to findings in other tissue types, complex I and complex II activity and maximal mitochondrial respiratory capacity in skeletal muscle were comparable between mKO mice and floxed/wild-type littermates. Moreover, there were no genotype differences in endurance exercise performance, skeletal muscle force generating capacity or the adaptive response of skeletal muscle to voluntary wheel running. Collectively, while we confirm the presence of STAT3 in skeletal muscle mitochondria, our data establishes that STAT3 is dispensable for mitochondrial and physiological function in skeletal muscle.
Labels: MiParea: Respiration, Genetic knockout;overexpression, Exercise physiology;nutrition;life style
Organism: Mouse Tissue;cell: Skeletal muscle Preparation: Permeabilized tissue
Coupling state: LEAK, OXPHOS, ET Pathway: F, N, S, NS, ROX HRR: Oxygraph-2k