Department

Departments of Kinesiology & Molecular Biology

First Advisor

Dr. Paul Thomas

Second Advisor

Dr. Mark Stayton

Description

Heart disease is the leading cause of death in the world, and one of the simplest measures that can be taken against it is aerobic exercise. Both exercise and a myocardial infarction (MI) can lead to hypertrophy of the heart. An MI leads to pathological growth, in contrast to the physiological growth caused by exercise. By examining the effects of training upon gene expression in the heart, we endeavor to understand how, and if, exercise may attenuate this response. To create a model system, C57BL/6J mice were obtained, and MIs were induced by surgically tying off the Left Anterior Descending (LAD) Coronary Artery. Once the mice recovered, they were trained on a treadmill for 8 weeks. Tissues were harvested, and RNA was isolated and checked fo r quality via capillary electrophoresis. Currently, RNA has been isolated from all of our samples, and is of ample quality for downstream applications. Our next step will be to run qPCR reactions to analyze the gene expression of markers for hypertrophy. T his assay will provide insight into the interactions of exercise and an MI, and how they influence cardiac hypertrophy. Future investigation will allow us to probe the changes within these signaling pathways more thoroughly.

Comments

Oral & Poster Presentation, Wyoming INBRE

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Effects of Aerobic Training on Gene Expression in the Heart after a Myocardial Infarctio

Heart disease is the leading cause of death in the world, and one of the simplest measures that can be taken against it is aerobic exercise. Both exercise and a myocardial infarction (MI) can lead to hypertrophy of the heart. An MI leads to pathological growth, in contrast to the physiological growth caused by exercise. By examining the effects of training upon gene expression in the heart, we endeavor to understand how, and if, exercise may attenuate this response. To create a model system, C57BL/6J mice were obtained, and MIs were induced by surgically tying off the Left Anterior Descending (LAD) Coronary Artery. Once the mice recovered, they were trained on a treadmill for 8 weeks. Tissues were harvested, and RNA was isolated and checked fo r quality via capillary electrophoresis. Currently, RNA has been isolated from all of our samples, and is of ample quality for downstream applications. Our next step will be to run qPCR reactions to analyze the gene expression of markers for hypertrophy. T his assay will provide insight into the interactions of exercise and an MI, and how they influence cardiac hypertrophy. Future investigation will allow us to probe the changes within these signaling pathways more thoroughly.