GSE159464
Chromatin accessibility data in  Wild Type and FGD5-AS1 knockdown CCC-HEH-2 cells (ATAC-Seq)
Purpose: According to the previous analysis results of gene regulation in fetal heart tissues with tetralogy of Fallot (ToF), we constructed the ceRNA mediated network driven by lncRNAs using a causal inference framework based on the expression correlations and validated miRNA-lncRNA/mRNA evidences. Totally 4 lncRNAs were identified as hub lncRNAs in the network, and FGD5-AS1 was focused for further loss-of-function investigation.   Methods: The specific shRNAs against FGD5-AS1 (sh-FGD5-AS1) as well as the corresponding negative control (sh-NC) were constructed along with lentiviral vector respectively. Then the CCC-HEH-2 human cardiac myocytes cell lines were infected with lentivirus and followed puromycin treatment for several days. The  knockdown efficiencies of the FGD5-AS1 expression were validated by qPCR.  The landscape of accessible chromatin in control and knockdown CCC-HEH-2 cell lines were observed using ATAC-Seq.  Conclusions:  Our data reveal a unique different chromatin state between wild type and FGD5-AS1 knockdown CCC-HEH-2 cells. Overall design: For CCC-HEH-2 cell line, 3 sh-NC cells and 3 sh-FGD5-AS1 cells were used and analyzed.