Analysis of Cardiac Function in BPTF KD Mice Using M-Mode Echocardiography

Yashi Agarwal

Faculty: Dr. Lauren Endres

Heart failure is one of the leading causes of premature death and disability in humans. Dilated cardiomyopathy (DCM) is the most common form of cardiac dysfunction and is diagnosed based on the dilation of the chambers of the heart and decreased cardiac output. DCM is largely regulated by chromatin remodeling complexes as they alter gene expression. There is a need to gain a better understanding of these complexes and how they directly affect cardiac health.

A major class of the SWI/SNF chromatin remodeling families is the NURF family. The largest subunit of NURF is bromodomain PHD finger transcription factor, or BPTF. In recent years, proteins containing bromodomains, of which there are 46, have gained popularity as targets for varying human diseases including inflammation and cardiovascular issues.

Research has been done to explore BPTF’s functional role in neurological disorders and tumor progression, but little is known regarding its part in cardiovascular-related disease phenotypes. The overall goal of this project is to thus investigate the role of BPTF, if any, in the context of chromatin remodeling as a response to dilated cardiomyopathy.

To investigate this in-vivo, we created cardiac myocyte-specific BPTF deletion C57BL/6 mice using tamoxifen-inducible Cre-LoxP technology, validated the identity of these mice using quantitative polymerase chain reaction (qPCR) based screening strategy, and used VevoLab Imaging Echocardiography to evaluate heart function for different variable including ejection fraction, fractional shortening, left ventricular internal diameter end diastole and left ventricular posterior wall end-diastole.