NOX2 inhibition impairs early muscle gene expression induced by a single exercise bout

NOX₂ inhibition impairs early muscle gene expression induced by a single exercise bout

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Standard

NOX₂ inhibition impairs early muscle gene expression induced by a single exercise bout. / Henríquez-Olguín, Carlos; Díaz-Vegas, Alexis; Utreras-Mendoza, Yildy; Campos, Cristian; Arias-Calderón, Manuel; Llanos, Paola; Contreras-Ferrat, Ariel; Espinosa, Alejandra; Altamirano, Francisco; Jaimovich, Enrique; Valladares, Denisse M.

I: Frontiers in Physiology, Bind 7, 282, 2016.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Henríquez-Olguín, C, Díaz-Vegas, A, Utreras-Mendoza, Y, Campos, C, Arias-Calderón, M, Llanos, P, Contreras-Ferrat, A, Espinosa, A, Altamirano, F, Jaimovich, E & Valladares, DM 2016, 'NOX₂ inhibition impairs early muscle gene expression induced by a single exercise bout', Frontiers in Physiology, bind 7, 282. https://doi.org/10.3389/fphys.2016.00282

APA

Henríquez-Olguín, C., Díaz-Vegas, A., Utreras-Mendoza, Y., Campos, C., Arias-Calderón, M., Llanos, P., Contreras-Ferrat, A., Espinosa, A., Altamirano, F., Jaimovich, E., & Valladares, D. M. (2016). NOX₂ inhibition impairs early muscle gene expression induced by a single exercise bout. Frontiers in Physiology, 7, [282]. https://doi.org/10.3389/fphys.2016.00282

Vancouver

Henríquez-Olguín C, Díaz-Vegas A, Utreras-Mendoza Y, Campos C, Arias-Calderón M, Llanos P o.a. NOX₂ inhibition impairs early muscle gene expression induced by a single exercise bout. Frontiers in Physiology. 2016;7. 282. https://doi.org/10.3389/fphys.2016.00282

Author

Henríquez-Olguín, Carlos ; Díaz-Vegas, Alexis ; Utreras-Mendoza, Yildy ; Campos, Cristian ; Arias-Calderón, Manuel ; Llanos, Paola ; Contreras-Ferrat, Ariel ; Espinosa, Alejandra ; Altamirano, Francisco ; Jaimovich, Enrique ; Valladares, Denisse M. / NOX₂ inhibition impairs early muscle gene expression induced by a single exercise bout. I: Frontiers in Physiology. 2016 ; Bind 7.

Bibtex

@article{d04bd2537b26435d8d0cb463803613a3,

title = "NOX2 inhibition impairs early muscle gene expression induced by a single exercise bout",

abstract = "Reactive oxygen species (ROS) participate as signaling molecules in response to exercise in skeletal muscle. However, the source of ROS and the molecular mechanisms involved in these phenomena are still not completely understood. The aim of this work was to study the role of skeletal muscle NADPH oxidase isoform 2 (NOX2) in the molecular response to physical exercise in skeletal muscle. BALB/c mice, pre-treated with a NOX2 inhibitor, apocynin, (3 mg/kg) or vehicle for 3 days, were swim-exercised for 60 min. Phospho-p47phox levels were significantly upregulated by exercise in flexor digitorum brevis (FDB). Moreover, exercise significantly increased NOX2 complex assembly (p47phox-gp91phox interaction) demonstrated by both proximity ligation assay and co-immunoprecipitation. Exercise-induced NOX2 activation was completely inhibited by apocynin treatment. As expected, exercise increased the mRNA levels of manganese superoxide dismutase (MnSOD), glutathione peroxidase (GPx), citrate synthase (CS), mitochondrial transcription factor A (tfam) and interleukin-6 (IL-I6) in FDB muscles. Moreover, the apocynin treatment was associated to a reduced activation of p38 MAP kinase, ERK 1/2, and NF-κB signaling pathways after a single bout of exercise. Additionally, the increase in plasma IL-6 elicited by exercise was decreased in apocynin-treated mice compared with the exercised vehicle-group (p < 0.001). These results were corroborated using gp91-dstat in an in vitro exercise model. In conclusion, NOX2 inhibition by both apocynin and gp91dstat, alters the intracellular signaling to exercise and electrical stimuli in skeletal muscle, suggesting that NOX2 plays a critical role in molecular response to an acute exercise.",

keywords = "Antioxidant defense, IL-6, Muscle adaptation, NADPH oxidase, Reactive oxygen species, Redox signaling",

author = "Carlos Henr{\'i}quez-Olgu{\'i}n and Alexis D{\'i}az-Vegas and Yildy Utreras-Mendoza and Cristian Campos and Manuel Arias-Calder{\'o}n and Paola Llanos and Ariel Contreras-Ferrat and Alejandra Espinosa and Francisco Altamirano and Enrique Jaimovich and Valladares, {Denisse M.}",

note = "Publisher Copyright: {\textcopyright} 2016 Henr{\'i}quez-Olgu{\'i}n, D{\'i}az-Vegas, Utreras-Mendoza, Campos, Arias-Calder{\'o}n, Llanos, Contreras-Ferrat, Espinosa, Altamirano, Jaimovich and Valladares.",

year = "2016",

doi = "10.3389/fphys.2016.00282",

language = "English",

volume = "7",

journal = "Frontiers in Physiology",

issn = "1664-042X",

publisher = "Frontiers Media S.A.",

}

RIS

TY - JOUR

T1 - NOX2 inhibition impairs early muscle gene expression induced by a single exercise bout

AU - Henríquez-Olguín, Carlos

AU - Díaz-Vegas, Alexis

AU - Utreras-Mendoza, Yildy

AU - Campos, Cristian

AU - Arias-Calderón, Manuel

AU - Llanos, Paola

AU - Contreras-Ferrat, Ariel

AU - Espinosa, Alejandra

AU - Altamirano, Francisco

AU - Jaimovich, Enrique

AU - Valladares, Denisse M.

PY - 2016

Y1 - 2016

N2 - Reactive oxygen species (ROS) participate as signaling molecules in response to exercise in skeletal muscle. However, the source of ROS and the molecular mechanisms involved in these phenomena are still not completely understood. The aim of this work was to study the role of skeletal muscle NADPH oxidase isoform 2 (NOX2) in the molecular response to physical exercise in skeletal muscle. BALB/c mice, pre-treated with a NOX2 inhibitor, apocynin, (3 mg/kg) or vehicle for 3 days, were swim-exercised for 60 min. Phospho-p47phox levels were significantly upregulated by exercise in flexor digitorum brevis (FDB). Moreover, exercise significantly increased NOX2 complex assembly (p47phox-gp91phox interaction) demonstrated by both proximity ligation assay and co-immunoprecipitation. Exercise-induced NOX2 activation was completely inhibited by apocynin treatment. As expected, exercise increased the mRNA levels of manganese superoxide dismutase (MnSOD), glutathione peroxidase (GPx), citrate synthase (CS), mitochondrial transcription factor A (tfam) and interleukin-6 (IL-I6) in FDB muscles. Moreover, the apocynin treatment was associated to a reduced activation of p38 MAP kinase, ERK 1/2, and NF-κB signaling pathways after a single bout of exercise. Additionally, the increase in plasma IL-6 elicited by exercise was decreased in apocynin-treated mice compared with the exercised vehicle-group (p < 0.001). These results were corroborated using gp91-dstat in an in vitro exercise model. In conclusion, NOX2 inhibition by both apocynin and gp91dstat, alters the intracellular signaling to exercise and electrical stimuli in skeletal muscle, suggesting that NOX2 plays a critical role in molecular response to an acute exercise.

AB - Reactive oxygen species (ROS) participate as signaling molecules in response to exercise in skeletal muscle. However, the source of ROS and the molecular mechanisms involved in these phenomena are still not completely understood. The aim of this work was to study the role of skeletal muscle NADPH oxidase isoform 2 (NOX2) in the molecular response to physical exercise in skeletal muscle. BALB/c mice, pre-treated with a NOX2 inhibitor, apocynin, (3 mg/kg) or vehicle for 3 days, were swim-exercised for 60 min. Phospho-p47phox levels were significantly upregulated by exercise in flexor digitorum brevis (FDB). Moreover, exercise significantly increased NOX2 complex assembly (p47phox-gp91phox interaction) demonstrated by both proximity ligation assay and co-immunoprecipitation. Exercise-induced NOX2 activation was completely inhibited by apocynin treatment. As expected, exercise increased the mRNA levels of manganese superoxide dismutase (MnSOD), glutathione peroxidase (GPx), citrate synthase (CS), mitochondrial transcription factor A (tfam) and interleukin-6 (IL-I6) in FDB muscles. Moreover, the apocynin treatment was associated to a reduced activation of p38 MAP kinase, ERK 1/2, and NF-κB signaling pathways after a single bout of exercise. Additionally, the increase in plasma IL-6 elicited by exercise was decreased in apocynin-treated mice compared with the exercised vehicle-group (p < 0.001). These results were corroborated using gp91-dstat in an in vitro exercise model. In conclusion, NOX2 inhibition by both apocynin and gp91dstat, alters the intracellular signaling to exercise and electrical stimuli in skeletal muscle, suggesting that NOX2 plays a critical role in molecular response to an acute exercise.

KW - Antioxidant defense

KW - IL-6

KW - Muscle adaptation

KW - NADPH oxidase

KW - Reactive oxygen species

KW - Redox signaling

UR - http://www.scopus.com/inward/record.url?scp=84981484980&partnerID=8YFLogxK

U2 - 10.3389/fphys.2016.00282

DO - 10.3389/fphys.2016.00282

M3 - Journal article

AN - SCOPUS:84981484980

VL - 7

JO - Frontiers in Physiology

JF - Frontiers in Physiology

SN - 1664-042X

M1 - 282

ER -

ID: 306300006