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Chronic ouabain prevents na,k-atpase dysfunction and targets ampk and il-6 in disused rat soleus muscle. / Kravtsova, Violetta V.; Paramonova, Inna I.; Vilchinskaya, Natalia A.; Tishkova, Maria V.; Matchkov, Vladimir V.; Shenkman, Boris S.; Krivoi, Igor I.

In: International Journal of Molecular Sciences, Vol. 22, No. 8, 3920, 10.04.2021.

Research output: Contribution to journalArticlepeer-review

Harvard

Kravtsova, VV, Paramonova, II, Vilchinskaya, NA, Tishkova, MV, Matchkov, VV, Shenkman, BS & Krivoi, II 2021, 'Chronic ouabain prevents na,k-atpase dysfunction and targets ampk and il-6 in disused rat soleus muscle', International Journal of Molecular Sciences, vol. 22, no. 8, 3920. https://doi.org/10.3390/ijms22083920

APA

Kravtsova, V. V., Paramonova, I. I., Vilchinskaya, N. A., Tishkova, M. V., Matchkov, V. V., Shenkman, B. S., & Krivoi, I. I. (2021). Chronic ouabain prevents na,k-atpase dysfunction and targets ampk and il-6 in disused rat soleus muscle. International Journal of Molecular Sciences, 22(8), [3920]. https://doi.org/10.3390/ijms22083920

Vancouver

Kravtsova VV, Paramonova II, Vilchinskaya NA, Tishkova MV, Matchkov VV, Shenkman BS et al. Chronic ouabain prevents na,k-atpase dysfunction and targets ampk and il-6 in disused rat soleus muscle. International Journal of Molecular Sciences. 2021 Apr 10;22(8). 3920. https://doi.org/10.3390/ijms22083920

Author

Kravtsova, Violetta V. ; Paramonova, Inna I. ; Vilchinskaya, Natalia A. ; Tishkova, Maria V. ; Matchkov, Vladimir V. ; Shenkman, Boris S. ; Krivoi, Igor I. / Chronic ouabain prevents na,k-atpase dysfunction and targets ampk and il-6 in disused rat soleus muscle. In: International Journal of Molecular Sciences. 2021 ; Vol. 22, No. 8.

BibTeX

@article{c18860a8dfe7433da6fd677200e8ffcb,
title = "Chronic ouabain prevents na,k-atpase dysfunction and targets ampk and il-6 in disused rat soleus muscle",
abstract = "Sustained sarcolemma depolarization due to loss of the Na,K-ATPase function is char-acteristic for skeletal muscle motor dysfunction. Ouabain, a specific ligand of the Na,K-ATPase, has a circulating endogenous analogue. We hypothesized that the Na,K-ATPase targeted by the elevated level of circulating ouabain modulates skeletal muscle electrogenesis and prevents its dis-use-induced disturbances. Isolated soleus muscles from rats intraperitoneally injected with oua-bain alone or subsequently exposed to muscle disuse by 6-h hindlimb suspension (HS) were stud-ied. Conventional electrophysiology, Western blotting, and confocal microscopy with cytochemis-try were used. Acutely applied 10 nM ouabain hyperpolarized the membrane. However, a single injection of ouabain (1 µg/kg) prior HS was unable to prevent the HS-induced membrane depo-larization. Chronic administration of ouabain for four days did not change the α1 and α2 Na,K-ATPase protein content, however it partially prevented the HS-induced loss of the Na,K-ATPase electrogenic activity and sarcolemma depolarization. These changes were associated with increased phosphorylation levels of AMP-activated protein kinase (AMPK), its substrate ac-etyl-CoA carboxylase and p70 protein, accompanied with increased mRNA expression of inter-leikin-6 (IL-6) and IL-6 receptor. Considering the role of AMPK in regulation of the Na,K-ATPase, we suggest an IL-6/AMPK contribution to prevent the effects of chronic ouabain under skeletal muscle disuse.",
keywords = "AMP-activated protein kinase, Hindlimb suspension, Na,K-ATPase isozymes, Ouabain, Resting membrane potential, Skeletal muscle, ouabain, Na, K-ATPase isozymes, resting membrane potential, hindlimb suspension, skeletal muscle",
author = "Kravtsova, {Violetta V.} and Paramonova, {Inna I.} and Vilchinskaya, {Natalia A.} and Tishkova, {Maria V.} and Matchkov, {Vladimir V.} and Shenkman, {Boris S.} and Krivoi, {Igor I.}",
note = "Publisher Copyright: {\textcopyright} 2021 by the authors. Licensee MDPI, Basel, Switzerland. Copyright: Copyright 2021 Elsevier B.V., All rights reserved.",
year = "2021",
month = apr,
day = "10",
doi = "10.3390/ijms22083920",
language = "English",
volume = "22",
journal = "International Journal of Molecular Sciences",
issn = "1422-0067",
publisher = "MDPI AG",
number = "8",

}

RIS

TY - JOUR

T1 - Chronic ouabain prevents na,k-atpase dysfunction and targets ampk and il-6 in disused rat soleus muscle

AU - Kravtsova, Violetta V.

AU - Paramonova, Inna I.

AU - Vilchinskaya, Natalia A.

AU - Tishkova, Maria V.

AU - Matchkov, Vladimir V.

AU - Shenkman, Boris S.

AU - Krivoi, Igor I.

N1 - Publisher Copyright: © 2021 by the authors. Licensee MDPI, Basel, Switzerland. Copyright: Copyright 2021 Elsevier B.V., All rights reserved.

PY - 2021/4/10

Y1 - 2021/4/10

N2 - Sustained sarcolemma depolarization due to loss of the Na,K-ATPase function is char-acteristic for skeletal muscle motor dysfunction. Ouabain, a specific ligand of the Na,K-ATPase, has a circulating endogenous analogue. We hypothesized that the Na,K-ATPase targeted by the elevated level of circulating ouabain modulates skeletal muscle electrogenesis and prevents its dis-use-induced disturbances. Isolated soleus muscles from rats intraperitoneally injected with oua-bain alone or subsequently exposed to muscle disuse by 6-h hindlimb suspension (HS) were stud-ied. Conventional electrophysiology, Western blotting, and confocal microscopy with cytochemis-try were used. Acutely applied 10 nM ouabain hyperpolarized the membrane. However, a single injection of ouabain (1 µg/kg) prior HS was unable to prevent the HS-induced membrane depo-larization. Chronic administration of ouabain for four days did not change the α1 and α2 Na,K-ATPase protein content, however it partially prevented the HS-induced loss of the Na,K-ATPase electrogenic activity and sarcolemma depolarization. These changes were associated with increased phosphorylation levels of AMP-activated protein kinase (AMPK), its substrate ac-etyl-CoA carboxylase and p70 protein, accompanied with increased mRNA expression of inter-leikin-6 (IL-6) and IL-6 receptor. Considering the role of AMPK in regulation of the Na,K-ATPase, we suggest an IL-6/AMPK contribution to prevent the effects of chronic ouabain under skeletal muscle disuse.

AB - Sustained sarcolemma depolarization due to loss of the Na,K-ATPase function is char-acteristic for skeletal muscle motor dysfunction. Ouabain, a specific ligand of the Na,K-ATPase, has a circulating endogenous analogue. We hypothesized that the Na,K-ATPase targeted by the elevated level of circulating ouabain modulates skeletal muscle electrogenesis and prevents its dis-use-induced disturbances. Isolated soleus muscles from rats intraperitoneally injected with oua-bain alone or subsequently exposed to muscle disuse by 6-h hindlimb suspension (HS) were stud-ied. Conventional electrophysiology, Western blotting, and confocal microscopy with cytochemis-try were used. Acutely applied 10 nM ouabain hyperpolarized the membrane. However, a single injection of ouabain (1 µg/kg) prior HS was unable to prevent the HS-induced membrane depo-larization. Chronic administration of ouabain for four days did not change the α1 and α2 Na,K-ATPase protein content, however it partially prevented the HS-induced loss of the Na,K-ATPase electrogenic activity and sarcolemma depolarization. These changes were associated with increased phosphorylation levels of AMP-activated protein kinase (AMPK), its substrate ac-etyl-CoA carboxylase and p70 protein, accompanied with increased mRNA expression of inter-leikin-6 (IL-6) and IL-6 receptor. Considering the role of AMPK in regulation of the Na,K-ATPase, we suggest an IL-6/AMPK contribution to prevent the effects of chronic ouabain under skeletal muscle disuse.

KW - AMP-activated protein kinase

KW - Hindlimb suspension

KW - Na,K-ATPase isozymes

KW - Ouabain

KW - Resting membrane potential

KW - Skeletal muscle

KW - ouabain

KW - Na

KW - K-ATPase isozymes

KW - resting membrane potential

KW - hindlimb suspension

KW - skeletal muscle

UR - http://www.scopus.com/inward/record.url?scp=85103834771&partnerID=8YFLogxK

U2 - 10.3390/ijms22083920

DO - 10.3390/ijms22083920

M3 - Article

C2 - 33920198

AN - SCOPUS:85103834771

VL - 22

JO - International Journal of Molecular Sciences

JF - International Journal of Molecular Sciences

SN - 1422-0067

IS - 8

M1 - 3920

ER -

ID: 77796425