Abstract:
Heart disease is the number one killer in the United States. Because this disease is such a prevalent killer, it is necessary to develop a better understanding of the protein pathways involved in the development of pathologic hypertrophy of the heart, which can lead to heart disease. Pathologic hypertrophy is an unhealthy type of enlargement of the tissue and arises from a pressure overload in the heart. Physiologic hypertrophy is a healthy type of hypertrophy and arises from a volume overload in the heart. The difference in the protein pathways involved in these two types of hypertrophy remains largely unknown. Perhaps there is a way to manipulate the proteins in a diseased heart to imitate physiologic hypertrophy in order to block the progression of heart disease. In this research project, a swim-training model was developed to induce cardiac hypertrophy in mice. Heart weight to body weight ratios (HW:BW) were collected for all of the hearts. Homogenates of these hypertrophied hearts as well as those of a control group were used for protein analysis. The difference in the phosphorylation state of Akt (a protein kinase involved in cell survival and cell growth) was determined for the control vs. swim-trained mice. The difference in the phosphorlyation state of p7OS6K (a protein that regulates cell growth and plays a role in the pathway to determination of cell size) also was determined for the control vs. swim-trained mice.
