mTOR-Notch3 signaling mediates pulmonary hypertension in hypoxia-exposed neonatal rats independent of changes in autophagy.
Identifieur interne : 000C82 ( Main/Exploration ); précédent : 000C81; suivant : 000C83mTOR-Notch3 signaling mediates pulmonary hypertension in hypoxia-exposed neonatal rats independent of changes in autophagy.
Auteurs : Julijana Ivanovska [Canada] ; Sparsh Shah [Canada] ; Mathew J. Wong [Canada] ; Crystal Kantores [Canada] ; Amish Jain [Canada] ; Martin Post [Canada] ; Behzad Yeganeh [Canada] ; Robert P. Jankov [Canada]Source :
- Pediatric pulmonology [ 1099-0496 ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux, Animaux nouveau-nés, Artère pulmonaire (métabolisme), Autophagie, Diamines (pharmacologie), Femelle, Hypertension pulmonaire (métabolisme), Hypoxie (métabolisme), Myocytes du muscle lisse (métabolisme), Mâle, Poumon (), Poumon (métabolisme), Prolifération cellulaire (), Rat Sprague-Dawley, Récepteur Notch3 (antagonistes et inhibiteurs), Récepteur Notch3 (métabolisme), Récepteur au PDGF bêta (métabolisme), Sirolimus (analogues et dérivés), Sirolimus (pharmacologie), Sérine-thréonine kinases TOR (antagonistes et inhibiteurs), Sérine-thréonine kinases TOR (métabolisme), Thiazoles (pharmacologie), Transduction du signal.
- MESH :
- analogues et dérivés : Sirolimus.
- antagonistes et inhibiteurs : Récepteur Notch3, Sérine-thréonine kinases TOR.
- métabolisme : Artère pulmonaire, Hypertension pulmonaire, Hypoxie, Myocytes du muscle lisse, Poumon, Récepteur Notch3, Récepteur au PDGF bêta, Sérine-thréonine kinases TOR.
- pharmacologie : Diamines, Sirolimus, Thiazoles.
- Animaux, Animaux nouveau-nés, Autophagie, Femelle, Mâle, Poumon, Prolifération cellulaire, Rat Sprague-Dawley, Transduction du signal.
English descriptors
- KwdEn :
- Animals, Animals, Newborn, Autophagy, Cell Proliferation (drug effects), Diamines (pharmacology), Female, Hypertension, Pulmonary (metabolism), Hypoxia (metabolism), Lung (blood supply), Lung (metabolism), Male, Myocytes, Smooth Muscle (metabolism), Pulmonary Artery (metabolism), Rats, Sprague-Dawley, Receptor, Notch3 (antagonists & inhibitors), Receptor, Notch3 (metabolism), Receptor, Platelet-Derived Growth Factor beta (metabolism), Signal Transduction, Sirolimus (analogs & derivatives), Sirolimus (pharmacology), TOR Serine-Threonine Kinases (antagonists & inhibitors), TOR Serine-Threonine Kinases (metabolism), Thiazoles (pharmacology).
- MESH :
- chemical , analogs & derivatives : Sirolimus.
- chemical , antagonists & inhibitors : Receptor, Notch3, TOR Serine-Threonine Kinases.
- chemical , metabolism : Receptor, Notch3, Receptor, Platelet-Derived Growth Factor beta, TOR Serine-Threonine Kinases.
- chemical , pharmacology : Diamines, Sirolimus, Thiazoles.
- blood supply : Lung.
- drug effects : Cell Proliferation.
- metabolism : Hypertension, Pulmonary, Hypoxia, Lung, Myocytes, Smooth Muscle, Pulmonary Artery.
- Animals, Animals, Newborn, Autophagy, Female, Male, Rats, Sprague-Dawley, Signal Transduction.
Abstract
Mammalian target of rapamycin (mTOR) is a pivotal regulator of cell proliferation, survival, and autophagy. Autophagy is increased in adult experimental chronic pulmonary hypertension (PHT), but its contributory role to pulmonary vascular disease remains uncertain and has yet to be explored in the neonatal animal. Notch is a major pro-proliferative pathway activated by mTOR. A direct relationship between autophagy and Notch signaling has not been previously explored. Our aim was to examine changes in mTOR-, Notch-, and autophagy-related pathways and the therapeutic effects of autophagy modulators in experimental chronic neonatal PHT secondary to chronic hypoxia.
DOI: 10.1002/ppul.23777
PubMed: 28759157
Affiliations:
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Le document en format XML
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<term>Animals, Newborn</term>
<term>Autophagy</term>
<term>Cell Proliferation (drug effects)</term>
<term>Diamines (pharmacology)</term>
<term>Female</term>
<term>Hypertension, Pulmonary (metabolism)</term>
<term>Hypoxia (metabolism)</term>
<term>Lung (blood supply)</term>
<term>Lung (metabolism)</term>
<term>Male</term>
<term>Myocytes, Smooth Muscle (metabolism)</term>
<term>Pulmonary Artery (metabolism)</term>
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<term>Receptor, Notch3 (antagonists & inhibitors)</term>
<term>Receptor, Notch3 (metabolism)</term>
<term>Receptor, Platelet-Derived Growth Factor beta (metabolism)</term>
<term>Signal Transduction</term>
<term>Sirolimus (analogs & derivatives)</term>
<term>Sirolimus (pharmacology)</term>
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<term>TOR Serine-Threonine Kinases (metabolism)</term>
<term>Thiazoles (pharmacology)</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Animaux nouveau-nés</term>
<term>Artère pulmonaire (métabolisme)</term>
<term>Autophagie</term>
<term>Diamines (pharmacologie)</term>
<term>Femelle</term>
<term>Hypertension pulmonaire (métabolisme)</term>
<term>Hypoxie (métabolisme)</term>
<term>Myocytes du muscle lisse (métabolisme)</term>
<term>Mâle</term>
<term>Poumon ()</term>
<term>Poumon (métabolisme)</term>
<term>Prolifération cellulaire ()</term>
<term>Rat Sprague-Dawley</term>
<term>Récepteur Notch3 (antagonistes et inhibiteurs)</term>
<term>Récepteur Notch3 (métabolisme)</term>
<term>Récepteur au PDGF bêta (métabolisme)</term>
<term>Sirolimus (analogues et dérivés)</term>
<term>Sirolimus (pharmacologie)</term>
<term>Sérine-thréonine kinases TOR (antagonistes et inhibiteurs)</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
<term>Thiazoles (pharmacologie)</term>
<term>Transduction du signal</term>
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<term>TOR Serine-Threonine Kinases</term>
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<term>Receptor, Platelet-Derived Growth Factor beta</term>
<term>TOR Serine-Threonine Kinases</term>
</keywords>
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<term>Sirolimus</term>
<term>Thiazoles</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Hypertension, Pulmonary</term>
<term>Hypoxia</term>
<term>Lung</term>
<term>Myocytes, Smooth Muscle</term>
<term>Pulmonary Artery</term>
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<term>Hypoxie</term>
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<term>Récepteur au PDGF bêta</term>
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<front><div type="abstract" xml:lang="en">Mammalian target of rapamycin (mTOR) is a pivotal regulator of cell proliferation, survival, and autophagy. Autophagy is increased in adult experimental chronic pulmonary hypertension (PHT), but its contributory role to pulmonary vascular disease remains uncertain and has yet to be explored in the neonatal animal. Notch is a major pro-proliferative pathway activated by mTOR. A direct relationship between autophagy and Notch signaling has not been previously explored. Our aim was to examine changes in mTOR-, Notch-, and autophagy-related pathways and the therapeutic effects of autophagy modulators in experimental chronic neonatal PHT secondary to chronic hypoxia.</div>
</front>
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<name sortKey="Kantores, Crystal" sort="Kantores, Crystal" uniqKey="Kantores C" first="Crystal" last="Kantores">Crystal Kantores</name>
<name sortKey="Post, Martin" sort="Post, Martin" uniqKey="Post M" first="Martin" last="Post">Martin Post</name>
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<name sortKey="Wong, Mathew J" sort="Wong, Mathew J" uniqKey="Wong M" first="Mathew J" last="Wong">Mathew J. Wong</name>
<name sortKey="Yeganeh, Behzad" sort="Yeganeh, Behzad" uniqKey="Yeganeh B" first="Behzad" last="Yeganeh">Behzad Yeganeh</name>
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