Presentation Type

Poster - Campus Access Only

Abstract

Duchenne Muscular Dystrophy (DMD) is an X-linked genetic disease that primarily affects young males. It causes progressive weakness of the skeletal and cardiac muscles, and is eventually fatal. While there are several existing therapeutic interventions for DMD, currently there is no cure. The purpose of this study was to measure initial cardiac physiological performance in the novel D2 dystrophic mouse model. The genotype of the mouse model utilized in this study contains the same spontaneous dystrophin gene mutation that DMD patients have, while maintaining possession of the utrophin-producing gene. The unique genetic makeup of the D2 mouse is believed to more accurately reflect the physiology and histology experienced by human DMD patients.

At four months old and prior to any therapeutic intervention, the D2 mice group

(n = 10) and the control group of D2J mice (n = 10) underwent technician-blinded echocardiograms while anesthetized, in order to assess the functionality of their cardiac muscle. Values acquired from these echocardiograms included cardiac output (CO), left ventricular mass (LVmass), percent ejection fraction (%EF), percent fractional shortening (%FS), and stroke volume (SV), to measure cardiac functionality levels.

When compared to the D2J mice, D2 mice did not demonstrate statistically significant differences in cardiac physiology. In future research, baseline cardiac measurements of these D2 mice can be compared to cardiac measurements from D2 mice treated in subsequent experiments, in order to evaluate the efficacy of new DMD supplementation and medication.

Category

Health and Medical Science

Available for download on Monday, April 20, 2020

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Apr 28th, 3:00 PM Apr 28th, 4:00 PM

Cardiac function in a novel dystrophic mouse model

UC South Ballroom

Duchenne Muscular Dystrophy (DMD) is an X-linked genetic disease that primarily affects young males. It causes progressive weakness of the skeletal and cardiac muscles, and is eventually fatal. While there are several existing therapeutic interventions for DMD, currently there is no cure. The purpose of this study was to measure initial cardiac physiological performance in the novel D2 dystrophic mouse model. The genotype of the mouse model utilized in this study contains the same spontaneous dystrophin gene mutation that DMD patients have, while maintaining possession of the utrophin-producing gene. The unique genetic makeup of the D2 mouse is believed to more accurately reflect the physiology and histology experienced by human DMD patients.

At four months old and prior to any therapeutic intervention, the D2 mice group

(n = 10) and the control group of D2J mice (n = 10) underwent technician-blinded echocardiograms while anesthetized, in order to assess the functionality of their cardiac muscle. Values acquired from these echocardiograms included cardiac output (CO), left ventricular mass (LVmass), percent ejection fraction (%EF), percent fractional shortening (%FS), and stroke volume (SV), to measure cardiac functionality levels.

When compared to the D2J mice, D2 mice did not demonstrate statistically significant differences in cardiac physiology. In future research, baseline cardiac measurements of these D2 mice can be compared to cardiac measurements from D2 mice treated in subsequent experiments, in order to evaluate the efficacy of new DMD supplementation and medication.