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. 2012 Aug 1;109(33):13362–13367. doi: 10.1073/pnas.1210906109

Fig. 1.

Fig. 1.

miR-138 and SIN3A regulate CFTR expression in airway epithelia. (A) SIN3A mRNA abundance in human primary airway epithelia at 24 h after the indicated interventions (n = 6). Scr, negative control; SIN3A DsiRNA, positive control; UnT, untransfected cells. (B) SIN3A protein abundance in primary airway epithelia at 72 h posttransfection. A representative immunoblot is shown. (C) CFTR mRNA abundance in Calu-3 cells at 24 h after indicated transfections. CFTR DsiRNA, positive control. (D) CFTR protein abundance in Calu-3 cells at 72 h posttransfection (R-769 antibody). (E and F) Changes in conductance (Gt) (E) and transepithelial current (It) (F) with indicated treatments. Basal resistance range, 397–586 ohm*cm2. Error bars indicate mean ± SE. *P < 0.01 relative to Scr; +P < 0.01, ++P < 0.01 relative to ΔGt and ΔIt in Scr-transfected samples on forskolin and IBMX (F&I) and CFTR inhibitor GlyH-101 treatment, respectively.