ArticleJournal of molecular and cellular cardiology2014
β-Adrenergic receptor-mediated transactivation of epidermal growth factor receptor decreases cardiomyocyte apoptosis through differential subcellular activation of ERK1/2 and Akt.
Article in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
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- Internalized β2-Adrenergic Receptors Oppose PLC-Dependent Hypertrophic Signaling.Circulation research · 2024Article
- Assessment of Tyrosine Kinase Inhibitors and Survival and Cardiovascular Outcomes of Patients With Non-Small Cell Lung Cancer in Taiwan.JAMA network open · 2023Article
- The association between tyrosine kinase inhibitors and fatal arrhythmia in patients with non-small cell lung cancer in Taiwan.Frontiers in oncology · 2023Article
- TRAIL and its receptors in cardiac diseases.Frontiers in physiology · 2023Review
- Epidermal growth factor receptor-dependent maintenance of cardiac contractility.Cardiovascular research · 2022Article
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- βJournal of molecular and cellular cardiology · 2021Article
- Transactivation of G protein-coupled receptors (GPCRs) and receptor tyrosine kinases (RTKs): Recent insights using luminescence and fluorescence technologies.Current opinion in endocrine and metabolic research · 2021Review
- A Dual Role for Death Receptor 5 in Regulating Cardiac Fibroblast Function.Frontiers in cardiovascular medicine · 2021Article
- β2-Adrenergic Receptors Increase Cardiac Fibroblast Proliferation Through the Gαs/ERK1/2-Dependent Secretion of Interleukin-6.International journal of molecular sciences · 2020Article
- Intravenous injection of extracellular vesicles to treat chronic myocardial ischemia.PloS one · 2020Article
- Death receptor 5 contributes to cardiomyocyte hypertrophy through epidermal growth factor receptor transactivation.Journal of molecular and cellular cardiology · 2019Article
- Protective transcriptional mechanisms in cardiomyocytes and cardiac fibroblasts.Journal of molecular and cellular cardiology · 2019Review
- Pepducin-mediated cardioprotection via β-arrestin-biased β2-adrenergic receptor-specific signaling.Theranostics · 2018Article
- Pyruvate enhancement of cardiac performance: Cellular mechanisms and clinical application.Experimental biology and medicine (Maywood, N.J.) · 2018Review
- Cardiac GPCR-Mediated EGFR Transactivation: Impact and Therapeutic Implications.Journal of cardiovascular pharmacology · 2017Review
- Leukocyte-Expressed β2-Adrenergic Receptors Are Essential for Survival After Acute Myocardial Injury.Circulation · 2016Article
- Time-dependent evolution of functional vs. remodeling signaling in induced pluripotent stem cell-derived cardiomyocytes and induced maturation with biomechanical stimulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
β-Adrenergic receptor (βAR)-mediated transactivation of epidermal growth factor receptor (EGFR) has been shown to relay pro-survival effects via unknown mechanisms. We hypothesized that acute βAR-mediated EGFR transactivation in the heart promotes differential subcellular activation of ERK1/2 and Akt, promoting cell survival through modulation of apoptosis. C57BL/6 mice underwent acute i.p. injection with isoproterenol (ISO)±AG 1478 (EGFR antagonist) to assess the impact of βAR-mediated EGFR transactivation on the phosphorylation of ERK1/2 (P-ERK1/2) and Akt (P-Akt) in distinct cardiac subcellular fractions. Increased P-ERK1/2 and P-Akt were observed in cytosolic, plasma membrane and nuclear fractions following ISO stimulation. Whereas the P-ERK1/2 response was EGFR-sensitive in all fractions, the P-Akt response was EGFR-sensitive only in the plasma membrane and nucleus, results confirmed in primary rat neonatal cardiomyocytes (RNCM). βAR-mediated EGFR-transactivation also decreased apoptosis in serum-depleted RNCM, as measured via TUNEL as well as caspase 3 activity/cleavage, which were sensitive to the inhibition of either ERK1/2 (PD184352) or Akt (LY-294002) signaling. Caspase 3 activity/cleavage was also sensitive to the inhibition of transcription, which, with an increase in nuclear P-ERK1/2 and P-Akt in response to ISO, suggested that βAR-mediated EGFR transactivation may regulate apoptotic gene transcription. An Apoptosis PCR Array identified tnfsf10 (TRAIL) to be altered by ISO in an EGFR-sensitive manner, results confirmed via RT-PCR and ELISA measurement of both membrane-bound and soluble cardiomyocyte TRAIL levels. βAR-mediated EGFR transactivation induces differential subcellular activation of ERK1/2 and Akt leading to increased cell survival through the modulation of caspase 3 activity and apoptotic gene expression in cardiomyocytes.
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Registered trials
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