Blocking airway mucous cell metaplasia by inhibiting EGFR antiapoptosis and IL-13 transdifferentiation signals
J. Clin. Invest. Jeffrey W. Tyner, et al. 116:309 doi:10.1172/JCI25167 [Go to this article.]

Figure 5
Effect of EGFR signaling pathways on apoptosis in airway epithelial cell cultures. (A) Representative photomicrogaphs of mTEC cultures that were treated with vehicle, PD153035 (0.3 μM), LY294002 (50 μM), and PD98059 (50 μM) for 3 days at 37°C and then subjected to immunofluorescent staining for cleaved fragment of active caspase-3 (act caspase-3) or TUNEL reaction. Scale bar: 20 μm. (B) Quantitative analysis of information in A for active caspase-3 staining cells (expressed as percentages of total Hoechst staining cells), using treatment conditions from A as well as PD15305 plus z-VAD-fmk (100 μM). (C) Immunoblot analysis of active caspase-3 and caspase-9 in cell lysates from mTEC cultures using treatment conditions from A. Anti–caspase-9 antibody recognizes precursor (caspase-9) and the cleaved fragment of active caspase-9. (D) Flow cytometric analysis of JC-1 staining of mTEC cultures using treatment conditions from A. Values represent percentages of cells with decreased mitochondrial membrane potential (ΔΨm) detected by shift from FL2 to FL1. For B and D, values represent mean ± SEM. *Significant difference from vehicle alone.