Cardiac-specific Depletion of Irf2bp2 Promotes Coronary Collateral Artery Formation in Female Mice

Aaron Farley

Faculty: Lauren Endres

Your genes are essentially chemical messages that are read by proteins to create other proteins that have an effect on everything that makes you an individual. Some of these proteins repress or activate the expression of other genes. Interferon Regulatory Factor 2 Binding Protein 2 (IRF2BP2) is one of these proteins.

We are asking the question of what role IRF2BP2 plays in the mouse heart. Our methods involve employing a gene recombination biotechnology system known as the CRE/loxP system to deplete Irf2bp2, disabling it from expressing. This western blot confirmed gene recombination procedure was completed on the parent generation of our conditional Irf2bp2 knockout (cKO) mouse line guaranteeing that the descendants would have the gene depleted.

We observed a significant increase in coronary arteries of appropriate size in the female cKO group in relation to the female wild type mouse. However, we did not observe a significant change in the cardiac capillary density nor did we observe any significant change in the male cKO group.

We were able to conclude that the depletion of Irf2bp2 expression promotes collateral coronary artery angiogenesis in the female mouse heart. These observations could play a role in decreasing the amount of tissue damage caused by myocardial infarctions in humans by allowing us to better understand how to genetically promote redundant collateral coronary artery angiogenesis.