Figure 1.

CSP7 mitigates MH and cilia shortening in AECs from COPD lungs. AECs isolated from nL and COPD lungs were treated with or without CSP7 or CP in vitro for 48 h. A: AEC lysates were immunoblotted for MUC5AC, HDAC6, FOXA2, FOXA3, SPDEF, acetylated tubulin (Ac-Tub), CAV1, p53, PAI-1, and LC3BII. Same samples were analyzed for β-actin to assess equal loading. Representative image from two independent experiments is shown. B: total RNA from AECs (n = 4) treated as in A were analyzed for MUC5AC, HDAC6, FOXA2, FOXA3, and CAV1 mRNA by qPCR. C: immunofluorescence staining (scale bar 500 µM and 200 µM) and colocalization of MUC5AC and HDAC6 in AECs from nL, and COPD lungs treated with or without CSP7. Representative image from two experiments is shown. Each experiment was repeated at least two to three times, and data are presented as means + SD and **P < 0.01 and ***P < 0.001 were obtained by one-way ANOVA with Tukey’s multiple comparison test and log-rank tests, respectively. AECs, airway epithelial cells; CAV1, caveolin‐1; COPD, chronic obstructive pulmonary disease; CSP7, caveolin-1 scaffolding domain peptide; FOXA2, forkhead box protein A2; HDAC6, histone deacetylase 6; MH, mucus hypersecretion; MUCAC, mucin 5AC; nL, “normal” lung; PAI-1, plasminogen activator inhibitor-1; SPDEF, domain-containing E26 transformation-specific like factor.