Gene expression analysis from bulk RNA isolated from embryonic mouse hearts at time points E13.5 and E14.5 with and without disruption of endothelial Ino80

Non-compaction cardiomyopathy is a devastating genetic disease caused by insufficient consolidation of ventricular wall muscle that can result in inadequate cardiac performance. Despite being the third most common cardiomyopathy, the mechanisms underlying the disease, including the cell types involved, are poorly understood. We explore the endothelial cell-specific deletion of the chromatin remodeler gene Ino80, which results in defective coronary vessel development that leads to ventricular non-compaction in embryonic mouse hearts. We observed a pathological endocardial cell population in the non-compacted hearts, and identified multiple dysregulated angiocrine factors that dramatically affected cardiomyocyte behavior. Overall design: Evaluation of 12 total samples, 3 each of WT and KO across 2 time points (E13.5 and E14.5)