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Thyroid hormone induces restrictive cardiomyopathy in β1-adrenoceptor knockout mice.
- Source :
-
Canadian Journal of Physiology & Pharmacology . Dec2023, Vol. 101 Issue 12, p620-629. 10p. - Publication Year :
- 2023
-
Abstract
- The purpose of this study was to characterize the role of β1-AR signaling and its cross-talk between cardiac renin–angiotensin system and thyroid-hormone-induced cardiac hypertrophy. T3 was administered at 0.5 mg·kg−1·day−1 for 10 days in β1-KOT3 and WTT3 groups, while control groups received vehicle alone. Echocardiography and myocardial histology was performed; cardiac and serum ANGI/ANGII and ANP and cardiac levels of p-PKA, p-ERK1/2, p-p38-MAPK, p-AKT, p-4EBP1, and ACE were measured. WTT3 showed decreased IVSTd and increased LVEDD versus WTsal (p < 0.05). β1-KOT3 exhibited lower LVEDD and higher relative IVSTd versus β1-KOsal, the lowest levels of ejection fraction, and the highest levels of cardiomyocyte diameter (p < 0.05). Cardiac ANP levels decreased in WTT3 versus β1-KOT3 (p < 0.05). Cardiac ACE expression was increased in T3-treated groups (p < 0.05). Phosphorylated-p38 MAPK levels were higher in WTT3 versus WTsal or β1-KOT3, p-4EBP1 was elevated in β1-KO animals, and p-ERK1/2 was up-regulated in β1-KOT3. These findings suggest that β1-AR signaling is crucial for TiCH. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 00084212
- Volume :
- 101
- Issue :
- 12
- Database :
- Academic Search Index
- Journal :
- Canadian Journal of Physiology & Pharmacology
- Publication Type :
- Academic Journal
- Accession number :
- 173978597
- Full Text :
- https://doi.org/10.1139/cjpp-2023-0153