ArticleAmerican journal of physiology. Heart and circulatory physiology2015
Temporal and gefitinib-sensitive regulation of cardiac cytokine expression via chronic β-adrenergic receptor stimulation.
Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- EGFR inhibition leads to enhanced desmosome assembly and cardiomyocyte cohesion via ROCK activation.JCI insight · 2023Article
- Epidermal growth factor receptor-dependent maintenance of cardiac contractility.Cardiovascular research · 2022Article
- Immune cell βAmerican journal of physiology. Heart and circulatory physiology · 2021Article
- Combined genetic and chemical screens indicate protective potential for EGFR inhibition to cardiomyocytes under hypoxia.Scientific reports · 2021Article
- β2-Adrenergic Receptors Increase Cardiac Fibroblast Proliferation Through the Gαs/ERK1/2-Dependent Secretion of Interleukin-6.International journal of molecular sciences · 2020Article
- Secreted Phospholipase ACells · 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
- Cardiac inflammatory CD11b/c cells exert a protective role in hypertrophied cardiomyocyte by promoting TNFRScientific reports · 2019Article
- Tumor Necrosis Factor-α in Heart Failure: an Updated Review.Current cardiology reports · 2018Review
- Cardiac fibroblast-specific p38α MAP kinase promotes cardiac hypertrophy via a putative paracrine interleukin-6 signaling mechanism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Proinflammatory Cytokines Mediate GPCR Dysfunction.Journal of cardiovascular pharmacology · 2017Review
- Cardiac GPCR-Mediated EGFR Transactivation: Impact and Therapeutic Implications.Journal of cardiovascular pharmacology · 2017Review
- Imatinib attenuates cardiac fibrosis by inhibiting platelet-derived growth factor receptors activation in isoproterenol induced model.PloS one · 2017Article
- Epidermal Growth Factor Receptor Transactivation: Mechanisms, Pathophysiology, and Potential Therapies in the Cardiovascular System.Annual review of pharmacology and toxicology · 2016Article
- Orphan Nuclear Receptor Nur77 Inhibits Cardiac Hypertrophic Response to Beta-Adrenergic Stimulation.Molecular and cellular biology · 2015Article
- Role of epidermal growth factor receptor and endoplasmic reticulum stress in vascular remodeling induced by angiotensin II.Hypertension (Dallas, Tex. : 1979) · 2015Article
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7 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic stimulation of β-adrenergic receptors (βAR) can promote survival signaling via transactivation of epidermal growth factor receptor (EGFR) but ultimately alters cardiac structure and contractility over time, in part via enhanced cytokine signaling. We hypothesized that chronic catecholamine signaling will have a temporal impact on cardiac transcript expression in vivo, in particular cytokines, and that EGFR transactivation plays a role in this process. C57BL/6 mice underwent infusion with vehicle or isoproterenol (Iso)±gefitinib (Gef) for 1 or 2 wk. Cardiac contractility decreased following 2 wk of Iso treatment, while cardiac hypertrophy, fibrosis, and apoptosis were enhanced at both timepoints. Inclusion of Gef preserved contractility, blocked Iso-induced apoptosis, and prevented hypertrophy at the 2-wk timepoint, but caused fibrosis on its own. RNAseq analysis revealed hundreds of cardiac transcripts altered by Iso at each timepoint with subsequent RT-quantitative PCR validation confirming distinct temporal patterns of transcript regulation, including those involved in cardiac remodeling and survival signaling, as well as numerous cytokines. Although Gef infusion alone did not significantly alter cytokine expression, it abrogated the Iso-mediated changes in a majority of the βAR-sensitive cytokines, including CCL2 and TNF-α. Additionally, the impact of βAR-dependent EGFR transactivation on the acute regulation of cytokine transcript expression was assessed in isolated cardiomyocytes and in cardiac fibroblasts, where the majority of Iso-dependent, and EGFR-sensitive, changes in cytokines occurred. Overall, coincident with changes in cardiac structure and contractility, βAR stimulation dynamically alters cardiac transcript expression over time, including numerous cytokines that are regulated via EGFR-dependent signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.