Skeletal muscle mitochondrial function and exercise capacity are not impaired in mice with knockout of STAT3
Autor: | Kristoffer Svensson, Shahriar Tahvilian, Carrie E. McCurdy, Keenan Greyslak, Simon Schenk, Byron Hetrick, Samuel LaBarge, Abha Sathe, Jessica R. Dent |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Male STAT3 Transcription Factor Physiology Mitochondrion Motor Activity Oxidative Phosphorylation 03 medical and health sciences Mice 0302 clinical medicine Muscular Diseases Physiology (medical) Physical Conditioning Animal medicine Animals Treadmill STAT3 Muscle Skeletal Mice Knockout Exercise Tolerance biology Chemistry Skeletal muscle Exercise capacity Electron transport chain Cell biology Mitochondria Muscle Mice Inbred C57BL 030104 developmental biology medicine.anatomical_structure STAT protein biology.protein 030217 neurology & neurosurgery Function (biology) Muscle Contraction Research Article |
Zdroj: | J Appl Physiol (1985) |
ISSN: | 1522-1601 |
Popis: | 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 although whether 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, although we confirm the presence of STAT3 in skeletal muscle mitochondria, our data establish that STAT3 is dispensable for mitochondrial and physiological function in skeletal muscle.NEW & NOTEWORTHY Whether signal transducer and activator of transcription 3 (STAT3) can regulate the activity of complex I and II of the electron transport chain and mitochondrial oxidative capacity in skeletal muscle, as it can in other tissues, is unknown. By using a mouse model lacking STAT3 in muscle, we demonstrate that skeletal muscle mitochondrial and physiological function, both in vivo and ex vivo, is not impacted by the loss of STAT3. |
Databáze: | OpenAIRE |
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