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Echocardiographic Approaches and Protocols for Comprehensive Phenotypic Characterization of Valvular Heart Disease in Mice
Published on: February 14, 2017
Characterization of the spontaneous degenerative mitral valve disease in FVB mice
Estelle Ayme-Dietrich1, Sylvia Da Silva1, Ghina Alame Bouabout2
1Laboratoire de Pharmacologie et Toxicologie NeuroCardiovasculaire UR7296, Fédération de Médecine Translationnelle, Centre Hospitalier Universitaire et Université de Strasbourg, Centre de Recherche en Biomédecine de Strasbourg (CRBS), Strasbourg, France.
Background:
The development of new non-surgical treatments dedicated to mitral valve degeneration is limited by the absence of relevant spontaneous and rapidly progressing animal experimental models.
Animals:
We characterized the spontaneous mitral valve degeneration in two inbred FVB mouse strains compared to C57BL/6J and investigated a contribution of the serotonergic system.
Methods:
Males and females FVB/NJ and FVB/NRj were compared to the putative C57BL/6J control at 12, 16, 20 and 24 weeks of age. Body weight, systolic blood pressure, heart rate, urinary 5-hydroxyindoleacetic acid (5-HIAA), whole blood and plasma serotonin, tail bleeding time, blood cell count, plasma TGF-β1 and plasma natriuretic peptide concentrations were measured. Myocardium and mitral valves were characterized by histology. mRNA mitral expression of 5-HT2A and 5-HT2B receptors was measured in the anterior leaflet. Cardiac anatomy and function were assessed by echocardiography.
Results:
Compared to C57BL/6J, FVB mice strains did not significantly differ regarding body weight increase, arterial blood pressure and heart rate. A progressive augmentation of plasma pro-ANP was observed in FVB mice. Nevertheless, no cardiac hypertrophy or left-ventricular fibrosis were observed. Accordingly, plasma TGF-β1 was not different among the three strains. Conversely, FVB mice demonstrated a high prevalence of fibromyxoid highly cellularized and enriched in glycosaminoglycans lesions, inducing major mitral leaflets thickening without increase in length. The increased thickness was correlated with urinary 5-HIAA and blood platelet count. Whole blood serotonin concentration was similar in the two strains but, in FVB, a reduction of plasma serotonin was observed together with an increase of the bleeding time. Finally, echocardiography identified left atrial and left ventricular remodeling associated with thickening of both mitral leaflets and mitral insufficient in 30% of FVB mice but no systolic protrusion of mitral leaflets towards the atrium.
Conclusion:
The FVB mouse strain is highly prone to spontaneous mitral myxomatous degeneration. A contribution of the peripheral serotonergic system is suggested.
Insights
The FVB mouse strain spontaneously develops mitral myxomatous degeneration, a condition potentially influenced by the serotonergic system. This finding aids in developing new non-surgical treatments for mitral valve disease.
Area of Science:
- Cardiovascular Research
- Translational Medicine
- Animal Models
Background:
- Developing non-surgical treatments for mitral valve degeneration requires suitable animal models.
- Current models often lack spontaneous and rapid progression of the disease.
Purpose of the Study:
- To characterize spontaneous mitral valve degeneration in FVB mouse strains.
- To compare FVB mice with C57BL/6J controls.
- To investigate the role of the serotonergic system in this degeneration.
Main Methods:
- Histological and echocardiographic analysis of FVB and C57BL/6J mice at various ages.
- Measurement of physiological parameters, blood markers (serotonin, TGF-β1, natriuretic peptide), and urinary 5-hydroxyindoleacetic acid (5-HIAA).
- Assessment of mitral valve histology and cardiac function.
Main Results:
- FVB mice exhibited significant mitral valve thickening due to fibromyxoid lesions, unlike C57BL/6J mice.
- This thickening correlated with urinary 5-HIAA and platelet count.
- FVB mice showed reduced plasma serotonin, increased bleeding time, and developed mitral insufficiency in 30% of cases.
Conclusions:
- The FVB mouse strain is a relevant model for spontaneous mitral myxomatous degeneration.
- The peripheral serotonergic system appears to contribute to the development of this condition.
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