ArticleJournal of receptor and signal transduction research2016
α1A-Adrenergic receptor prevents cardiac ischemic damage through PKCδ/GLUT1/4-mediated glucose uptake.
Article in Journal of receptor and signal transduction research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- The alpha-1A adrenergic receptor regulates mitochondrial oxidative metabolism in the mouse heart.Journal of molecular and cellular cardiology · 2024Article
- An arrayed CRISPR knockout screen identifies genetic regulators of GLUT1 expression.Scientific reports · 2023Article
- αInternational journal of molecular sciences · 2023Review
- Characterization of a novel positive allosteric modulator of the αCurrent research in pharmacology and drug discovery · 2023Article
- Theory and Applications of the (Cardio) Genomic Fabric Approach to Post-Ischemic and Hypoxia-Induced Heart Failure.Journal of personalized medicine · 2022Article
- Sympatho-adrenergic mechanisms in heart failure: new insights into pathophysiology.Medical review (2021) · 2021Article
- Review
- Targeting Adrenergic Receptors in Metabolic Therapies for Heart Failure.International journal of molecular sciences · 2021Review
- αJournal of receptor and signal transduction research · 2021Article
- Current Developments on the Role of αFrontiers in cell and developmental biology · 2021Review
- A comparison of the metabolic side-effects of the second-generation antipsychotic drugs risperidone and paliperidone in animal models.PloS one · 2021Article
- Mitochondrial Metabolism in Myocardial Remodeling and Mechanical Unloading: Implications for Ischemic Heart Disease.Frontiers in cardiovascular medicine · 2021Review
- Changes in Myocardial Metabolism Preceding Sudden Cardiac Death.Frontiers in physiology · 2020Review
- Correlation of GLUT1 and GLUT4 with prognosis of patients with hypothyroidism and cardiac insufficiency.American journal of cardiovascular disease · 2020Article
- Adrenoceptor regulation of the mechanistic target of rapamycin in muscle and adipose tissue.British journal of pharmacology · 2019Review
- The role of αJournal of receptor and signal transduction research · 2017Article
- Novel Structural Approaches to Study GPCR Regulation.International journal of molecular sciences · 2016Review
- Enhancement of Glucose Metabolism via PGC-1α Participates in the Cardioprotection of Chronic Intermittent Hypobaric Hypoxia.Frontiers in physiology · 2016Article
- Central Circadian Clock Regulates Energy Metabolism.Advances in experimental medicine and biologyReview
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3 authors.
Funding
Abstract
While α(1)-adrenergic receptors (ARs) have been previously shown to limit ischemic cardiac damage, the mechanisms remain unclear. Most previous studies utilized low oxygen conditions in addition to ischemic buffers with glucose deficiencies, but we discovered profound differences if the two conditions are separated. We assessed both mouse neonatal and adult myocytes and HL-1 cells in a series of assays assessing ischemic damage under hypoxic or low glucose conditions. We found that α(1)-AR stimulation protected against increased lactate dehydrogenase release or Annexin V(+) apoptosis under conditions that were due to low glucose concentration not to hypoxia. The α(1)-AR antagonist prazosin or nonselective protein kinase C (PKC) inhibitors blocked the protective effect. α(1)-AR stimulation increased (3)H-deoxyglucose uptake that was blocked with either an inhibitor to glucose transporter 1 or 4 (GLUT1 or GLUT4) or small interfering RNA (siRNA) against PKCδ. GLUT1/4 inhibition also blocked α(1)-AR-mediated protection from apoptosis. The PKC inhibitor rottlerin or siRNA against PKCδ blocked α(1)-AR stimulated GLUT1 or GLUT4 plasma membrane translocation. α(1)-AR stimulation increased plasma membrane concentration of either GLUT1 or GLUT4 in a time-dependent fashion. Transgenic mice overexpressing the α(1A)-AR but not α(1B)-AR mice displayed increased glucose uptake and increased GLUT1 and GLUT4 plasma membrane translocation in the adult heart while α(1A)-AR but not α(1B)-AR knockout mice displayed lowered glucose uptake and GLUT translocation. Our results suggest that α(1)-AR activation is anti-apoptotic and protective during cardiac ischemia due to glucose deprivation and not hypoxia by enhancing glucose uptake into the heart via PKCδ-mediated GLUT translocation that may be specific to the α(1A)-AR subtype.
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