Abid 2020 FASEB J: Difference between revisions
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{{Publication | {{Publication | ||
|title=Abid H, Ryan ZC, Delmotte P, Sieck GC, Lanza IR (2020) Extramyocellular interleukin-6 influences skeletal muscle mitochondrial physiology through canonical JAK/STAT signaling pathways. FASEB J | |title=Abid H, Ryan ZC, Delmotte P, Sieck GC, Lanza IR (2020) Extramyocellular interleukin-6 influences skeletal muscle mitochondrial physiology through canonical JAK/STAT signaling pathways. FASEB J 34:14458-72. | ||
|info=[https://www.ncbi.nlm.nih.gov/pubmed/32885495 PMID: 32885495 Open Access] | |info=[https://www.ncbi.nlm.nih.gov/pubmed/32885495 PMID: 32885495 Open Access] | ||
|authors=Abid | |authors=Abid Hinnah, Ryan Zachary C, Delmotte Philippe, Sieck Gary C, Lanza Ian R | ||
|year=2020 | |year=2020 | ||
|journal=FASEB J | |journal=FASEB J | ||
|abstract=Interleukin-6 (IL-6) is a pleiotropic cytokine that has been shown to be produced acutely by skeletal muscle in response to exercise, yet chronically elevated with obesity and aging. The mechanisms by which IL-6 influences skeletal muscle mitochondria acutely and chronically are unclear. To better understand the influence of extramyocellular IL-6 on skeletal muscle mitochondrial physiology, we treated differentiated myotubes with exogenous IL-6 to evaluate the dose- and duration-dependent effects of IL-6 on salient aspects of mitochondrial biology and the role of canonical IL-6 signaling in muscle cells. Acute exposure of myotubes to IL-6 increased the mitochondrial reactive oxygen species (mtROS) production and oxygen consumption rates ( | |abstract=Interleukin-6 (IL-6) is a pleiotropic cytokine that has been shown to be produced acutely by skeletal muscle in response to exercise, yet chronically elevated with obesity and aging. The mechanisms by which IL-6 influences skeletal muscle mitochondria acutely and chronically are unclear. To better understand the influence of extramyocellular IL-6 on skeletal muscle mitochondrial physiology, we treated differentiated myotubes with exogenous IL-6 to evaluate the dose- and duration-dependent effects of IL-6 on salient aspects of mitochondrial biology and the role of canonical IL-6 signaling in muscle cells. Acute exposure of myotubes to IL-6 increased the mitochondrial reactive oxygen species (mtROS) production and oxygen consumption rates (JO<sub>2</sub>) in a manner that was dependent on activation of the JAK/STAT pathway. Furthermore, STAT3 activation by IL-6 was partly attenuated by MitoQ, a mitochondrial-targeted antioxidant, suggesting that mtROS potentiates STAT3 signaling in skeletal muscle in response to IL-6 exposure. In concert with effects on mitochondrial physiology, acute IL-6 exposure induced several mitochondrial adaptations, consistent with the stress-induced mitochondrial hyperfusion. Exposure of myotubes to chronically elevated IL-6 further increased mtROS with eventual loss of respiratory capacity. These data provide new evidence supporting the interplay between cytokine signaling and mitochondrial physiology in skeletal muscle. | ||
|keywords=STAT3, Interleukin-6, Mitochondria, Reactive oxygen species, Skeletal muscle | |keywords=STAT3, Interleukin-6, Mitochondria, Reactive oxygen species, Skeletal muscle | ||
|editor=[[Plangger M]] | |editor=[[Plangger M]] | ||
|mipnetlab=US MN Rochester Nair KS | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration | |area=Respiration, Pharmacology;toxicology | ||
|instruments=Oxygraph-2k | |injuries=Oxidative stress;RONS | ||
|additional=2020-09 | |organism=Mouse | ||
|tissues=Skeletal muscle | |||
|preparations=Intact cells | |||
|couplingstates=LEAK, OXPHOS | |||
|pathways=N, S, NS | |||
|instruments=Oxygraph-2k, O2k-Fluorometer | |||
|additional=2020-09, AmR | |||
}} | }} |
Latest revision as of 20:46, 6 November 2020
Abid H, Ryan ZC, Delmotte P, Sieck GC, Lanza IR (2020) Extramyocellular interleukin-6 influences skeletal muscle mitochondrial physiology through canonical JAK/STAT signaling pathways. FASEB J 34:14458-72. |
Abid Hinnah, Ryan Zachary C, Delmotte Philippe, Sieck Gary C, Lanza Ian R (2020) FASEB J
Abstract: Interleukin-6 (IL-6) is a pleiotropic cytokine that has been shown to be produced acutely by skeletal muscle in response to exercise, yet chronically elevated with obesity and aging. The mechanisms by which IL-6 influences skeletal muscle mitochondria acutely and chronically are unclear. To better understand the influence of extramyocellular IL-6 on skeletal muscle mitochondrial physiology, we treated differentiated myotubes with exogenous IL-6 to evaluate the dose- and duration-dependent effects of IL-6 on salient aspects of mitochondrial biology and the role of canonical IL-6 signaling in muscle cells. Acute exposure of myotubes to IL-6 increased the mitochondrial reactive oxygen species (mtROS) production and oxygen consumption rates (JO2) in a manner that was dependent on activation of the JAK/STAT pathway. Furthermore, STAT3 activation by IL-6 was partly attenuated by MitoQ, a mitochondrial-targeted antioxidant, suggesting that mtROS potentiates STAT3 signaling in skeletal muscle in response to IL-6 exposure. In concert with effects on mitochondrial physiology, acute IL-6 exposure induced several mitochondrial adaptations, consistent with the stress-induced mitochondrial hyperfusion. Exposure of myotubes to chronically elevated IL-6 further increased mtROS with eventual loss of respiratory capacity. These data provide new evidence supporting the interplay between cytokine signaling and mitochondrial physiology in skeletal muscle. โข Keywords: STAT3, Interleukin-6, Mitochondria, Reactive oxygen species, Skeletal muscle โข Bioblast editor: Plangger M โข O2k-Network Lab: US MN Rochester Nair KS
Labels: MiParea: Respiration, Pharmacology;toxicology
Stress:Oxidative stress;RONS Organism: Mouse Tissue;cell: Skeletal muscle Preparation: Intact cells
Coupling state: LEAK, OXPHOS
Pathway: N, S, NS
HRR: Oxygraph-2k, O2k-Fluorometer
2020-09, AmR