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Echocardiographic and Histological Examination of Cardiac Morphology in the Mouse
Published on: October 26, 2017
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Mouse models for the study of postnatal cardiac hypertrophy
A Del Olmo-Turrubiarte1,2, A Calzada-Torres1, G Díaz-Rosas1
1Laboratorio de Investigación de Biología del Desarrollo y Teratogénesis Experimental, Hospital Infantil de México Federico Gómez (HIMFG), Mexico.
International Journal of Cardiology. Heart & Vasculature
|August 9, 2017
Summary
This study developed a new postnatal model for cardiac hypertrophy (CH) in mice. The findings highlight adrenergic receptors and GATA4 as key factors in developing pathological CH in early life.
Area of Science:
- Cardiovascular Research
- Developmental Biology
- Pathology
Background:
- Childhood cardiac hypertrophy (CH) mechanisms remain incompletely understood.
- Existing models may not fully recapitulate early-onset pathological CH.
Purpose of the Study:
- To establish a novel postnatal animal model for studying cardiac hypertrophy (CH).
- To elucidate the molecular mechanisms underlying pathological CH in early developmental stages.
Main Methods:
- Pregnant mice received intraperitoneal isoproterenol (ISO) for 7 days.
- Offspring were analyzed at various developmental stages (fetal, newborn, neonate, young adult).
- Histopathology, immunohistochemistry, Western blot, and qPCR were employed to assess cardiac structure and gene/protein expression.
Main Results:
- ISO administration induced significant structural changes in offspring hearts, including increased ventricular wall and septal size.
- Histopathology revealed loss of cellular compaction and fibrous foci in the left ventricle.
- Increased expression of adrenergic receptors and GATA4 was observed, with GATA4 implicated as a determining factor in pathology.
Conclusions:
- A new, effective postnatal animal model for pathological cardiac hypertrophy (CH) was successfully established.
- Adrenergic receptors may initiate the transition from physiological to pathological hypertrophy.
- GATA4 appears to be a critical determinant in the development of pathological CH.
