ArticleBMC pharmacology & toxicology2014
Cardiac thromboxane A2 receptor activation does not directly induce cardiomyocyte hypertrophy but does cause cell death that is prevented with gentamicin and 2-APB.
Article in BMC pharmacology & toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- 12(S)-HETE regulates the expression of IL-6 and IL-10 in cardiomyocytes through two distinct receptors, TXA2R and BLT2.Biochemistry and biophysics reports · 2026Article
- Thrombaxane-B2 as a predictor marker of atrial fibrillation.International journal of cardiology. Cardiovascular risk and prevention · 2026Article
- Burns: The "Fuse" That Ignites Organ Crisis - A Narrative Review of Mechanisms and Crosstalk in Post-Burn MODS.Journal of inflammation research · 2026Review
- Doxorubicin alters G-protein coupled receptor-mediated vasocontraction in rat coronary arteries.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Adjustment for Renal Function Improves the Prognostic Performance of Urinary Thromboxane Metabolites.Clinical chemistry · 2024Article
- Gemcitabine resistance in non-small cell lung cancer is mediated through activation of the PI3K/AKT/NF-κB pathway and suppression of ERK signaling by reactive oxygen species.Journal of biochemical and molecular toxicology · 2023Article
- The Link between Prostanoids and Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Nonplatelet thromboxane generation is associated with impaired cardiovascular performance and mortality in heart failure.American journal of physiology. Heart and circulatory physiology · 2022Article
- Bitter Taste Receptors as Regulators of Abdominal Muscles Contraction.Physiological research · 2019Article
- Antagonism of the Thromboxane-Prostanoid Receptor as a Potential Therapy for Cardiomyopathy of Muscular Dystrophy.Journal of the American Heart Association · 2019Article
- Lipopolysaccharide (LPS)-induced septic shock causes profound changes in myocardial energy metabolites in pigs.Metabolomics : Official journal of the Metabolomic Society · 2018Article
- Antagonism of the thromboxane-prostanoid receptor is cardioprotective against right ventricular pressure overload.Pulmonary circulation · 2016Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe have previously shown that the thromboxane (TXA2) receptor agonist, U46619, can directly induce ventricular arrhythmias that were associated with increases in intracellular calcium in cardiomyocytes. Since TXA2 is an inflammatory mediator and induces direct calcium changes in cardiomyocytes, we hypothesized that TXA2 released during ischemia or inflammation could also cause cardiac remodeling.
methodsU46619 (0.1-10 μM) was applied to isolated adult mouse ventricular primary cardiomyocytes, mouse ventricular cardiac muscle strips, and cultured HL-1 cardiomyocytes and markers of hypertrophy and cell death were measured.
resultsWe found that TXA2 receptors were expressed in ventricular cardiomyocytes and were functional via calcium imaging. U46619 treatment for 24 h did not increase expression of pathological hypertrophy genes (atrial natriuretic peptide, β-myosin heavy chain, skeletal muscle α-actin) and it did not increase protein synthesis. There was also no increase in cardiomyocyte size after 48 h treatment with U46619 as measured by flow cytometry. However, U46619 (0.1-10 μM) caused a concentration-dependent increase in cardiomyocyte death (trypan blue, MTT assays, visual cell counts and TUNEL stain) after 24 h. Treatment of cells with the TXA2 receptor antagonist SQ29548 and inhibitors of the IP3 pathway, gentamicin and 2-APB, eliminated the increase in cell death induced by U46619.
conclusionsOur data suggests that TXA2 does not induce cardiac hypertrophy, but does induce cell death that is mediated in part by IP3 signaling pathways. These findings may provide important therapeutic targets for inflammatory-induced cardiac apoptosis that can lead to heart failure.
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