Description
We reprogrammed fibroblasts from 5 HLHS patients and 2 controls into iPSCs and differentiated into cardiomyocytes. By comparison of HLHS and control groups we uncovered the developmental, structural and functional defects of HLHS cells. Through high through-put screening, the underlying molecular mechnisms of HLHS ontology was explored. Overall design: Cardiomyocyte mRNA profiles of normal control and HLHS samples were generated by deep sequencing, in duplicate, using Illumina HiSeq4000.