ArticleMolecular and cellular biochemistry2012
Β-adrenergic receptor stimulation induces endoplasmic reticulum stress in adult cardiac myocytes: role in apoptosis.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 58 citations in OpenAlex.
- Beta-adrenergic stimulation promotes an endoplasmic reticulum stress-dependent inflammatory program in salivary gland epithelial cells.Clinical and experimental immunology · 2024Article
- Adipocyte-released adipomes in Chagas cardiomyopathy: Impact on cardiac metabolic and immune regulation.iScience · 2024Article
- Mechanism ofCancers · 2023Article
- Timolol maleate, a β blocker eye drop, improved edema in a retinal vein occlusion model.Molecular vision · 2023Article
- Lipid Dyshomeostasis and Inherited Cerebellar Ataxia.Molecular neurobiology · 2022Review
- Importance of Autophagy in Mediating Cellular Responses to Iron Overload in Cardiomyocytes.Reviews in cardiovascular medicine · 2022Review
- Biology of Cardiac Troponins: Emphasis on Metabolism.Biology · 2022Review
- Ero1α-Dependent ERp44 Dissociation From RyR2 Contributes to Cardiac Arrhythmia.Circulation research · 2022Article
- Metabolic Pathway of Cardiospecific Troponins: From Fundamental Aspects to Diagnostic Role (Comprehensive Review).Frontiers in molecular biosciences · 2022Review
- ER stress and calcium-dependent arrhythmias.Frontiers in physiology · 2022Review
- The Importance of Cardiac Troponin Metabolism in the Laboratory Diagnosis of Myocardial Infarction (Comprehensive Review).BioMed research international · 2022Review
- Cardioprotective Potential of Exogenous Ubiquitin.Cardiovascular drugs and therapy · 2021Review
- Activation of ER stress signalling increases mortality after a major trauma.Journal of cellular and molecular medicine · 2020Article
- Intermittent Hypoxia Triggers Early Cardiac Remodeling and Contractile Dysfunction in the Time-Course of Ischemic Cardiomyopathy in Rats.Journal of the American Heart Association · 2020Article
- Curcumin attenuates hypoxia/reoxygenation‑induced myocardial injury.Molecular medicine reports · 2019Article
- Long noncoding RNA UCA1 inhibits ischaemia/reperfusion injury induced cardiomyocytes apoptosis via suppression of endoplasmic reticulum stress.Genes & genomics · 2019Article
- Endoplasmic reticulum stress in the heart: insights into mechanisms and drug targets.British journal of pharmacology · 2018Review
- NF2 signaling pathway plays a pro-apoptotic role in β-adrenergic receptor stimulated cardiac myocyte apoptosis.PloS one · 2018Article
- SIRT1 protects the heart from ER stress-induced cell death through eIF2α deacetylation.Cell death and differentiation · 2017Article
- Osteopontin: At the cross-roads of myocyte survival and myocardial function.Life sciences · 2014Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Accumulation of misfolded proteins and alterations in calcium homeostasis induces endoplasmic reticulum (ER) stress, leading to apoptosis. In this study, we tested the hypothesis that β-AR stimulation induces ER stress, and induction of ER stress plays a pro-apoptotic role in cardiac myocytes. Using thapsigargin and brefeldin A, we demonstrate that ER stress induces apoptosis in adult rat ventricular myocytes (ARVMs). β-AR-stimulation (isoproterenol; 3h) significantly increased expression of ER stress proteins, such as GRP-78, Gadd-153, and Gadd-34, while activating caspase-12 in ARVMs. In most parts, these effects were mimicked by thapsigargin. β-AR stimulation for 15 min increased PERK and eIF-2α phosphorylation. PERK phosphorylation remained higher, while eIF-2α phosphorylation declined thereafter, reaching to ~50% below basal levels at 3 h after β-AR stimulation. This decline in eIF-2α phosphorylation was prevented by β1-AR, not by β2-AR antagonist. Forskolin, adenylyl cyclase activator, simulated the effects of ISO on eIF-2α phosphorylation. Salubrinal (SAL), an ER stress inhibitor, maintained eIF-2α phosphorylation and inhibited β-AR-stimulated apoptosis. Furthermore, inhibition of caspase-12 using z-ATAD inhibited β-AR-stimulated and thapsigargin-induced apoptosis. In vivo, β-AR stimulation induced ER stress in the mouse heart as evidenced by increased expression of GRP-78 and Gadd-153, activation of caspase-12, and dephosphorylation of eIF-2α. SAL maintained phosphorylation of eIF-2α, inhibited activation of caspase-12, and decreased β-AR-stimulated apoptosis in the heart. Thus, β-AR stimulation induces ER stress in cardiac myocytes and in the heart, and induction of ER stress plays a pro-apoptotic role.
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Registered trials
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