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Thromboxane A2 mimetic, U46619, does not induce markers of pathological hypertrophy in cardiomyocytes
Author(s) -
Wacker Michael J,
Tchikrizov Vladimir,
Swan Hannah K,
Wetmore Lori A,
Touchberry Chad D
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1128.7
Subject(s) - muscle hypertrophy , thromboxane a2 , medicine , endocrinology , myocyte , atrial natriuretic peptide , thromboxane , chemistry , receptor , platelet
We have previously shown that application of the thromboxane (TxA2) receptor agonist, U46619 , induces increases in intracellular calcium in isolated primary cardiomyocytes. One of the well‐known effects of sustained increases in intracellular calcium in cardiomyocytes is pathological hypertrophy. Since TxA2 is an inflammatory mediator, we hypothesized that TxA2 release during inflammation would result in cardiac hypertrophy. U46619 (0.1–10 μM) was applied to isolated primary mouse cardiomyocytes, cardiac muscle strips, and cultured HL‐1 cardiomyocytes and markers of hypertrophy were measured. U46619 treatment for 24 hrs did not increase expression of pathological hypertrophy genes (atrial natriuretic peptide, beta myosin heavy chain, skeletal muscle alpha actin) and it did not increase protein synthesis. There was also no increase in HL‐1 cardiomyocyte cell size after 48 hr treatment with U46619 as measured by flow cytometry. Previous reports have suggested that cyclooxygenase products such as TxA2 may play a role in directly inducing hypertrophy and cardiac remodeling. However, our current data would suggest that TxA2 at the doses and times we tested does not induce markers of pathological hypertrophy. (Support was provided by American Heart Association 11SDG5330016 to MJW)