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Difference between revisions of "Abid 2020 FASEB J"

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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 [Epub ahead of print].
|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 H, Ryan ZC, Delmotte P, Sieck GC, Lanza IR
|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 (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.
|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 19:46, 6 November 2020

Publications in the MiPMap
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.

Β» PMID: 32885495 Open Access

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. β€’ Keywords: STAT3, Interleukin-6, Mitochondria, Reactive oxygen species, Skeletal muscle β€’ Bioblast editor: Plangger M β€’ 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