Downregulation of epithelial sodium channel (ENaC) activity in cystic fibrosis cells by epigenetic targeting.

ABSTRACT: The pathogenic mechanism of cystic fibrosis (CF) includes the functional interaction of the cystic fibrosis transmembrane conductance regulator (CFTR) protein with the epithelial sodium channel (ENaC). The reduction of ENaC activity may constitute a therapeutic option for CF. This hypothesis was evaluated using drugs that target the protease-dependent activation of the ENaC channel and the transcriptional activity of its coding genes. To this aim we used: camostat, a protease inhibitor; S-adenosyl methionine (SAM), showed to induce DNA hypermethylation; curcumin, known to produce chromatin condensation. SAM and camostat are drugs already clinically used in other pathologies, while curcumin is a common dietary compound. The experimental systems used were CF and non-CF immortalized human bro

SUBMITTER: Blacona G 

PROVIDER: S-EPMC9035428 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature