Adverse transverse-tubule remodeling in a rat model of heart failure is attenuated with low-dose triiodothyronine treatment

Pre-clinical animal studies have shown that triiodothyronine (T3) replacement therapy improves cardiac contractile function after myocardial infarction (MI). We hypothesized that T3 treatment could prevent adverse post-infarction cardiomyocyte remodeling by maintaining transverse-tubule (TT) structu...

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Bibliographic Details
Published in:Molecular medicine (Cambridge, Mass.) Mass.), 2019-12, Vol.25 (1), p.53-53, Article 53
Main Authors: An, Shimin, Gilani, Nimra, Huang, Yuan, Muncan, Adam, Zhang, Youhua, Tang, Yi-Da, Gerdes, A Martin, Ojamaa, Kaie
Format: Article
Language:English
Subjects:
Calcium transients
Cardiac arrhythmia
Cardiac function
Cardiomyocytes
Cardiovascular disease
Contractility
Coronary vessels
Drinking water
Heart attacks
Heart failure
Hormone replacement therapy
Hypothyroidism
Laboratory animals
Mortality
Ostomy
Surgery
T-tubules
Thyroid gland
Triiodothyronine
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Summary:Pre-clinical animal studies have shown that triiodothyronine (T3) replacement therapy improves cardiac contractile function after myocardial infarction (MI). We hypothesized that T3 treatment could prevent adverse post-infarction cardiomyocyte remodeling by maintaining transverse-tubule (TT) structures, thus improving calcium dynamics and contractility. METHODS: Myocardial infarction (MI) or sham surgeries were performed on female Sprague-Dawley rats (aged 12 wks), followed by treatment with T3 (5μg/kg/d) or vehicle in drinking water for 16 wks (n = 10-11/group). After in vivo echocardiographic and hemodynamic analyses, left ventricular myocytes were isolated by collagenase digestion and simultaneous calcium and contractile transients in single cardiomyocytes were recorded using IonOptix imaging. Live cardiomyocytes were stained with AlexaFluor-488 conjugated wheat germ agglutinin (WGA-488) or di-8-ANEPPS, and multiple z-stack images per cell were captured by confocal microscopy for analysis of TT organization. RTqPCR and immunoblot approaches determined expression of TT proteins. RESULTS: Echocardiography and in vivo hemodynamic measurements showed significant improvements in systolic and diastolic function in T3- vs vehicle-treated MI rats. Isolated cardiomyocyte analysis showed significant dysfunction in measurements of myocyte relengthening in MI hearts, and improvements with T3 treatment: max relengthening velocity (Vmax, um/s), 2.984 ± 1.410 vs 1.593 ± 0.325, p 
ISSN:1076-1551
1528-3658
DOI:10.1186/s10020-019-0120-3