GlutaredoxinV1, Main, Exploration, bibRecord, 000486

β3-Adrenoceptor activation relieves oxidative inhibition of the cardiac Na+-K+ pump in hyperglycemia induced by insulin receptor blockade.

Identifieur interne : 000486 ( Main/Exploration ); précédent : 000485; suivant : 000487

β3-Adrenoceptor activation relieves oxidative inhibition of the cardiac Na+-K+ pump in hyperglycemia induced by insulin receptor blockade.

Auteurs : Keyvan Karimi Galougahi [Australie] ; Chia-Chi Liu [Australie] ; Alvaro Garcia [Australie] ; Natasha A. Fry [Australie] ; Elisha J. Hamilton [Australie] ; Gemma A. Figtree [Australie] ; Helge H. Rasmussen [Australie]

Source :

American journal of physiology. Cell physiology [ 1522-1563 ] ; 2015.

RBID : pubmed:26063704

Descripteurs français

KwdFr :
- Agonistes des récepteurs bêta-3 adrénergiques (pharmacologie), Agonistes des récepteurs bêta-3 adrénergiques (usage thérapeutique), Animaux (MeSH), Dioxoles (pharmacologie), Dioxoles (usage thérapeutique), Données de séquences moléculaires (MeSH), Glycémie (effets des médicaments et des substances chimiques), Glycémie (métabolisme), Hyperglycémie (métabolisme), Hyperglycémie (traitement médicamenteux), Lapins (MeSH), Mâle (MeSH), Récepteur à l'insuline (antagonistes et inhibiteurs), Récepteurs bêta-3 adrénergiques (métabolisme), Sodium-Potassium-Exchanging ATPase (antagonistes et inhibiteurs), Stress oxydatif (effets des médicaments et des substances chimiques), Stress oxydatif (physiologie), Séquence d'acides aminés (MeSH).
MESH :
- antagonistes et inhibiteurs : Récepteur à l'insuline, Sodium-Potassium-Exchanging ATPase.
- effets des médicaments et des substances chimiques : Glycémie, Stress oxydatif.
- métabolisme : Glycémie, Hyperglycémie, Récepteurs bêta-3 adrénergiques.
- pharmacologie : Agonistes des récepteurs bêta-3 adrénergiques, Dioxoles.
- physiologie : Stress oxydatif.
- traitement médicamenteux : Hyperglycémie.
- usage thérapeutique : Agonistes des récepteurs bêta-3 adrénergiques, Dioxoles.
- Animaux, Données de séquences moléculaires, Lapins, Mâle, Séquence d'acides aminés.

English descriptors

KwdEn :
- Adrenergic beta-3 Receptor Agonists (pharmacology), Adrenergic beta-3 Receptor Agonists (therapeutic use), Amino Acid Sequence (MeSH), Animals (MeSH), Blood Glucose (drug effects), Blood Glucose (metabolism), Dioxoles (pharmacology), Dioxoles (therapeutic use), Hyperglycemia (drug therapy), Hyperglycemia (metabolism), Male (MeSH), Molecular Sequence Data (MeSH), Oxidative Stress (drug effects), Oxidative Stress (physiology), Rabbits (MeSH), Receptor, Insulin (antagonists & inhibitors), Receptors, Adrenergic, beta-3 (metabolism), Sodium-Potassium-Exchanging ATPase (antagonists & inhibitors).
MESH :
- chemical , antagonists & inhibitors : Receptor, Insulin, Sodium-Potassium-Exchanging ATPase.
- chemical , drug effects : Blood Glucose.
- chemical , metabolism : Blood Glucose, Receptors, Adrenergic, beta-3.
- chemical , pharmacology : Adrenergic beta-3 Receptor Agonists, Dioxoles.
- chemical , therapeutic use : Adrenergic beta-3 Receptor Agonists, Dioxoles.
- drug effects : Oxidative Stress.
- drug therapy : Hyperglycemia.
- metabolism : Hyperglycemia.
- physiology : Oxidative Stress.
- Amino Acid Sequence, Animals, Male, Molecular Sequence Data, Rabbits.

Abstract

Dysregulated nitric oxide (NO)- and superoxide (O2 (·-))-dependent signaling contributes to the pathobiology of diabetes-induced cardiovascular complications. We examined if stimulation of β3-adrenergic receptors (β3-ARs), coupled to endothelial NO synthase (eNOS) activation, relieves oxidative inhibition of eNOS and the Na(+)-K(+) pump induced by hyperglycemia. Hyperglycemia was established in male New Zealand White rabbits by infusion of the insulin receptor antagonist S961 for 7 days. Hyperglycemia increased tissue and blood indexes of oxidative stress. It induced glutathionylation of the Na(+)-K(+) pump β1-subunit in cardiac myocytes, an oxidative modification causing pump inhibition, and reduced the electrogenic pump current in voltage-clamped myocytes. Hyperglycemia also increased glutathionylation of eNOS, which causes its uncoupling, and increased coimmunoprecipitation of cytosolic p47(phox) and membranous p22(phox) NADPH oxidase subunits, consistent with NADPH oxidase activation. Blocking translocation of p47(phox) to p22(phox) with the gp91ds-tat peptide in cardiac myocytes ex vivo abolished the hyperglycemia-induced increase in glutathionylation of the Na(+)-K(+) pump β1-subunit and decrease in pump current. In vivo treatment with the β3-AR agonist CL316243 for 3 days eliminated the increase in indexes of oxidative stress, decreased coimmunoprecipitation of p22(phox) with p47(phox), abolished the hyperglycemia-induced increase in glutathionylation of eNOS and the Na(+)-K(+) pump β1-subunit, and abolished the decrease in pump current. CL316243 also increased coimmunoprecipitation of glutaredoxin-1 with the Na(+)-K(+) pump β1-subunit, which may reflect facilitation of deglutathionylation. In vivo β3-AR activation relieves oxidative inhibition of key cardiac myocyte proteins in hyperglycemia and may be effective in targeting the deleterious cardiac effects of diabetes.

DOI: 10.1152/ajpcell.00071.2015
PubMed: 26063704
PubMed Central: PMC4556897

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<term>Adrenergic beta-3 Receptor Agonists (therapeutic use)</term>
<term>Amino Acid Sequence (MeSH)</term>
<term>Animals (MeSH)</term>
<term>Blood Glucose (drug effects)</term>
<term>Blood Glucose (metabolism)</term>
<term>Dioxoles (pharmacology)</term>
<term>Dioxoles (therapeutic use)</term>
<term>Hyperglycemia (drug therapy)</term>
<term>Hyperglycemia (metabolism)</term>
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<term>Molecular Sequence Data (MeSH)</term>
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<term>Oxidative Stress (physiology)</term>
<term>Rabbits (MeSH)</term>
<term>Receptor, Insulin (antagonists & inhibitors)</term>
<term>Receptors, Adrenergic, beta-3 (metabolism)</term>
<term>Sodium-Potassium-Exchanging ATPase (antagonists & inhibitors)</term>
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<term>Agonistes des récepteurs bêta-3 adrénergiques (usage thérapeutique)</term>
<term>Animaux (MeSH)</term>
<term>Dioxoles (pharmacologie)</term>
<term>Dioxoles (usage thérapeutique)</term>
<term>Données de séquences moléculaires (MeSH)</term>
<term>Glycémie (effets des médicaments et des substances chimiques)</term>
<term>Glycémie (métabolisme)</term>
<term>Hyperglycémie (métabolisme)</term>
<term>Hyperglycémie (traitement médicamenteux)</term>
<term>Lapins (MeSH)</term>
<term>Mâle (MeSH)</term>
<term>Récepteur à l'insuline (antagonistes et inhibiteurs)</term>
<term>Récepteurs bêta-3 adrénergiques (métabolisme)</term>
<term>Sodium-Potassium-Exchanging ATPase (antagonistes et inhibiteurs)</term>
<term>Stress oxydatif (effets des médicaments et des substances chimiques)</term>
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<term>Molecular Sequence Data</term>
<term>Rabbits</term>
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<term>Données de séquences moléculaires</term>
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<front><div type="abstract" xml:lang="en">Dysregulated nitric oxide (NO)- and superoxide (O2 (·-))-dependent signaling contributes to the pathobiology of diabetes-induced cardiovascular complications. We examined if stimulation of β3-adrenergic receptors (β3-ARs), coupled to endothelial NO synthase (eNOS) activation, relieves oxidative inhibition of eNOS and the Na(+)-K(+) pump induced by hyperglycemia. Hyperglycemia was established in male New Zealand White rabbits by infusion of the insulin receptor antagonist S961 for 7 days. Hyperglycemia increased tissue and blood indexes of oxidative stress. It induced glutathionylation of the Na(+)-K(+) pump β1-subunit in cardiac myocytes, an oxidative modification causing pump inhibition, and reduced the electrogenic pump current in voltage-clamped myocytes. Hyperglycemia also increased glutathionylation of eNOS, which causes its uncoupling, and increased coimmunoprecipitation of cytosolic p47(phox) and membranous p22(phox) NADPH oxidase subunits, consistent with NADPH oxidase activation. Blocking translocation of p47(phox) to p22(phox) with the gp91ds-tat peptide in cardiac myocytes ex vivo abolished the hyperglycemia-induced increase in glutathionylation of the Na(+)-K(+) pump β1-subunit and decrease in pump current. In vivo treatment with the β3-AR agonist CL316243 for 3 days eliminated the increase in indexes of oxidative stress, decreased coimmunoprecipitation of p22(phox) with p47(phox), abolished the hyperglycemia-induced increase in glutathionylation of eNOS and the Na(+)-K(+) pump β1-subunit, and abolished the decrease in pump current. CL316243 also increased coimmunoprecipitation of glutaredoxin-1 with the Na(+)-K(+) pump β1-subunit, which may reflect facilitation of deglutathionylation. In vivo β3-AR activation relieves oxidative inhibition of key cardiac myocyte proteins in hyperglycemia and may be effective in targeting the deleterious cardiac effects of diabetes. </div>
</front>
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<DateCompleted><Year>2015</Year>
<Month>11</Month>
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<DateRevised><Year>2020</Year>
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<Title>American journal of physiology. Cell physiology</Title>
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<ArticleTitle>β3-Adrenoceptor activation relieves oxidative inhibition of the cardiac Na+-K+ pump in hyperglycemia induced by insulin receptor blockade.</ArticleTitle>
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<Abstract><AbstractText>Dysregulated nitric oxide (NO)- and superoxide (O2 (·-))-dependent signaling contributes to the pathobiology of diabetes-induced cardiovascular complications. We examined if stimulation of β3-adrenergic receptors (β3-ARs), coupled to endothelial NO synthase (eNOS) activation, relieves oxidative inhibition of eNOS and the Na(+)-K(+) pump induced by hyperglycemia. Hyperglycemia was established in male New Zealand White rabbits by infusion of the insulin receptor antagonist S961 for 7 days. Hyperglycemia increased tissue and blood indexes of oxidative stress. It induced glutathionylation of the Na(+)-K(+) pump β1-subunit in cardiac myocytes, an oxidative modification causing pump inhibition, and reduced the electrogenic pump current in voltage-clamped myocytes. Hyperglycemia also increased glutathionylation of eNOS, which causes its uncoupling, and increased coimmunoprecipitation of cytosolic p47(phox) and membranous p22(phox) NADPH oxidase subunits, consistent with NADPH oxidase activation. Blocking translocation of p47(phox) to p22(phox) with the gp91ds-tat peptide in cardiac myocytes ex vivo abolished the hyperglycemia-induced increase in glutathionylation of the Na(+)-K(+) pump β1-subunit and decrease in pump current. In vivo treatment with the β3-AR agonist CL316243 for 3 days eliminated the increase in indexes of oxidative stress, decreased coimmunoprecipitation of p22(phox) with p47(phox), abolished the hyperglycemia-induced increase in glutathionylation of eNOS and the Na(+)-K(+) pump β1-subunit, and abolished the decrease in pump current. CL316243 also increased coimmunoprecipitation of glutaredoxin-1 with the Na(+)-K(+) pump β1-subunit, which may reflect facilitation of deglutathionylation. In vivo β3-AR activation relieves oxidative inhibition of key cardiac myocyte proteins in hyperglycemia and may be effective in targeting the deleterious cardiac effects of diabetes. </AbstractText>
<CopyrightInformation>Copyright © 2015 the American Physiological Society.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Karimi Galougahi</LastName>
<ForeName>Keyvan</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>North Shore Heart Research Group, Kolling Institute, University of Sydney, Sydney, Australia; and Department of Cardiology, Royal North Shore Hospital, Sydney, Australia.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Chia-Chi</ForeName>
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   |texte=   β3-Adrenoceptor activation relieves oxidative inhibition of the cardiac Na+-K+ pump in hyperglycemia induced by insulin receptor blockade.
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β3-Adrenoceptor activation relieves oxidative inhibition of the cardiac Na+-K+ pump in hyperglycemia induced by insulin receptor blockade.

β3-Adrenoceptor activation relieves oxidative inhibition of the cardiac Na+-K+ pump in hyperglycemia induced by insulin receptor blockade.

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