CHAC1 Is Differentially Expressed in Normal and Cystic Fibrosis Bronchial Epithelial Cells and Regulates the Inflammatory Response Induced by Pseudomonas aeruginosa

Perra, Léa; Balloy, Viviane; Foussignière, Tobias; Moissenet, Didier; Petat, Hortense; Mungrue, Imran N.; Touqui, Lhousseine; Corvol, Harriet; Chignard, Michel; Guillot, Loic

Next, we examined CHAC1 protein expression in response to Pa stimulation. Consistent with previous reports indicating that CHAC1 protein is very unstable due to its rapid degradation by the proteasome in Neuro2a cells (23), we were unable to detect endogenous CHAC1 protein in NCI-H292 at baseline (Supplementary Figure 2B) or after Pa infection (data not shown). Additionally, we were unable to detect CHAC1 protein expression after treating the cells with tunicamycin, a known inducer of CHAC1 mRNA expression (24) (data not shown). CHAC1 was only detected at the protein level when it was either overexpressed with a plasmid in NCI-H292 cells (Figure 2E ) or when the cells were treated with at least 1 µM of the proteasome inhibitor MG-132 ( Figure 2F ).