Increased tolerance to stress in cardiac expressed gain-of-function of adenosine triphosphate-sensitive potassium channel subunit Kir6.1.
Identifieur interne : 000F70 ( Main/Exploration ); précédent : 000F69; suivant : 000F71Increased tolerance to stress in cardiac expressed gain-of-function of adenosine triphosphate-sensitive potassium channel subunit Kir6.1.
Auteurs : Matthew C. Henn [États-Unis] ; M Burhan Janjua [États-Unis] ; Haixia Zhang [États-Unis] ; Evelyn M. Kanter [États-Unis] ; Carol M. Makepeace [États-Unis] ; Richard B. Schuessler [États-Unis] ; Colin G. Nichols [États-Unis] ; Jennifer S. Lawton [États-Unis]Source :
- The Journal of surgical research [ 1095-8673 ] ; 2016.
Descripteurs français
- KwdFr :
- Animaux, Canaux KATP (génétique), Canaux KATP (physiologie), Cardiomégalie (génétique), Cardiomégalie (physiopathologie), Diazoxide (pharmacologie), Hypertrichose (génétique), Hypertrichose (physiopathologie), Marqueurs génétiques, Mutation, Myocytes cardiaques (), Myocytes cardiaques (physiologie), Ostéochondrodysplasies (génétique), Ostéochondrodysplasies (physiopathologie), Souris, Souris transgéniques, Stress physiologique (), Stress physiologique (physiologie), Taille de la cellule (), Vasodilatateurs (pharmacologie).
- MESH :
- génétique : Canaux KATP, Cardiomégalie, Hypertrichose, Ostéochondrodysplasies.
- pharmacologie : Diazoxide, Vasodilatateurs.
- physiologie : Canaux KATP, Myocytes cardiaques, Stress physiologique.
- physiopathologie : Cardiomégalie, Hypertrichose, Ostéochondrodysplasies.
- Animaux, Marqueurs génétiques, Mutation, Myocytes cardiaques, Souris, Souris transgéniques, Stress physiologique, Taille de la cellule.
English descriptors
- KwdEn :
- Animals, Cardiomegaly (genetics), Cardiomegaly (physiopathology), Cell Size (drug effects), Diazoxide (pharmacology), Genetic Markers, Hypertrichosis (genetics), Hypertrichosis (physiopathology), KATP Channels (genetics), KATP Channels (physiology), Mice, Mice, Transgenic, Mutation, Myocytes, Cardiac (drug effects), Myocytes, Cardiac (physiology), Osteochondrodysplasias (genetics), Osteochondrodysplasias (physiopathology), Stress, Physiological (drug effects), Stress, Physiological (physiology), Vasodilator Agents (pharmacology).
- MESH :
- chemical , genetics : KATP Channels.
- chemical , pharmacology : Diazoxide, Vasodilator Agents.
- drug effects : Cell Size, Myocytes, Cardiac, Stress, Physiological.
- genetics : Cardiomegaly, Hypertrichosis, Osteochondrodysplasias.
- chemical , physiology : KATP Channels, Myocytes, Cardiac, Stress, Physiological.
- physiopathology : Cardiomegaly, Hypertrichosis, Osteochondrodysplasias.
- Animals, Genetic Markers, Mice, Mice, Transgenic, Mutation.
Abstract
The adenosine triphosphate-sensitive potassium (KATP) channel opener diazoxide (DZX) prevents myocyte volume derangement and reduced contractility secondary to stress. KATP channels are composed of pore-forming (Kir6.1 or Kir6.2) and regulatory (sulfonylurea receptor, SUR1 or SUR2) subunits. Gain of function (GOF) of Kir6.1 subunits has been implicated in cardiac pathology in Cantu syndrome in humans (cardiomegaly, lymphedema, and pericardial effusions). We hypothesized that GOF of Kir6.1 subunits would result in altered myocyte response to stress.
DOI: 10.1016/j.jss.2016.08.043
PubMed: 27884343
Affiliations:
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Le document en format XML
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<term>Cardiomegaly (genetics)</term>
<term>Cardiomegaly (physiopathology)</term>
<term>Cell Size (drug effects)</term>
<term>Diazoxide (pharmacology)</term>
<term>Genetic Markers</term>
<term>Hypertrichosis (genetics)</term>
<term>Hypertrichosis (physiopathology)</term>
<term>KATP Channels (genetics)</term>
<term>KATP Channels (physiology)</term>
<term>Mice</term>
<term>Mice, Transgenic</term>
<term>Mutation</term>
<term>Myocytes, Cardiac (drug effects)</term>
<term>Myocytes, Cardiac (physiology)</term>
<term>Osteochondrodysplasias (genetics)</term>
<term>Osteochondrodysplasias (physiopathology)</term>
<term>Stress, Physiological (drug effects)</term>
<term>Stress, Physiological (physiology)</term>
<term>Vasodilator Agents (pharmacology)</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Canaux KATP (génétique)</term>
<term>Canaux KATP (physiologie)</term>
<term>Cardiomégalie (génétique)</term>
<term>Cardiomégalie (physiopathologie)</term>
<term>Diazoxide (pharmacologie)</term>
<term>Hypertrichose (génétique)</term>
<term>Hypertrichose (physiopathologie)</term>
<term>Marqueurs génétiques</term>
<term>Mutation</term>
<term>Myocytes cardiaques ()</term>
<term>Myocytes cardiaques (physiologie)</term>
<term>Ostéochondrodysplasies (génétique)</term>
<term>Ostéochondrodysplasies (physiopathologie)</term>
<term>Souris</term>
<term>Souris transgéniques</term>
<term>Stress physiologique ()</term>
<term>Stress physiologique (physiologie)</term>
<term>Taille de la cellule ()</term>
<term>Vasodilatateurs (pharmacologie)</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>KATP Channels</term>
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<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Diazoxide</term>
<term>Vasodilator Agents</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Size</term>
<term>Myocytes, Cardiac</term>
<term>Stress, Physiological</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cardiomegaly</term>
<term>Hypertrichosis</term>
<term>Osteochondrodysplasias</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Canaux KATP</term>
<term>Cardiomégalie</term>
<term>Hypertrichose</term>
<term>Ostéochondrodysplasies</term>
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<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Diazoxide</term>
<term>Vasodilatateurs</term>
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<term>Stress physiologique</term>
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<term>Myocytes, Cardiac</term>
<term>Stress, Physiological</term>
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<term>Hypertrichose</term>
<term>Ostéochondrodysplasies</term>
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<term>Osteochondrodysplasias</term>
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<term>Mutation</term>
<term>Myocytes cardiaques</term>
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<front><div type="abstract" xml:lang="en">The adenosine triphosphate-sensitive potassium (KATP) channel opener diazoxide (DZX) prevents myocyte volume derangement and reduced contractility secondary to stress. KATP channels are composed of pore-forming (Kir6.1 or Kir6.2) and regulatory (sulfonylurea receptor, SUR1 or SUR2) subunits. Gain of function (GOF) of Kir6.1 subunits has been implicated in cardiac pathology in Cantu syndrome in humans (cardiomegaly, lymphedema, and pericardial effusions). We hypothesized that GOF of Kir6.1 subunits would result in altered myocyte response to stress.</div>
</front>
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<affiliations><list><country><li>États-Unis</li>
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<tree><country name="États-Unis"><region name="Missouri (État)"><name sortKey="Henn, Matthew C" sort="Henn, Matthew C" uniqKey="Henn M" first="Matthew C" last="Henn">Matthew C. Henn</name>
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<name sortKey="Janjua, M Burhan" sort="Janjua, M Burhan" uniqKey="Janjua M" first="M Burhan" last="Janjua">M Burhan Janjua</name>
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<name sortKey="Lawton, Jennifer S" sort="Lawton, Jennifer S" uniqKey="Lawton J" first="Jennifer S" last="Lawton">Jennifer S. Lawton</name>
<name sortKey="Makepeace, Carol M" sort="Makepeace, Carol M" uniqKey="Makepeace C" first="Carol M" last="Makepeace">Carol M. Makepeace</name>
<name sortKey="Nichols, Colin G" sort="Nichols, Colin G" uniqKey="Nichols C" first="Colin G" last="Nichols">Colin G. Nichols</name>
<name sortKey="Schuessler, Richard B" sort="Schuessler, Richard B" uniqKey="Schuessler R" first="Richard B" last="Schuessler">Richard B. Schuessler</name>
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