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. 2020 Jan 15;318(3):L483–L493. doi: 10.1152/ajplung.00212.2019

Fig. 2.

Fig. 2.

Exposure to tunicamycin activates the protein kinase RNA-like endoplasmic reticulum kinase (PERK)/ eukaryotic initiation factor 2α (eIF2α) pathway in airway smooth muscle (ASM) cells. A: 12-h exposure to tunicamycin significantly increased total PERK expression [relative to ribosomal protein S16 (RPS16)] in ASM cells compared with untreated controls. Representative Western blots are shown. B: 12-h exposure to tunicamycin significantly increased the ratio of phosphorylated to total eIF2α in ASM cells compared with untreated controls. Representative Western blots are shown. C: exposure to tunicamycin did not significantly change total eIF2α expression (relative to RPS16) in ASM cells compared with untreated controls. Data are presented as medians and interquartile range (IQR) represented as a box-and-whisker plot. Results were analyzed using a 2-way ANOVA. Untreated controls for each time point were performed. *Significant difference (P < 0.05) compared with untreated control (n = 5 patients).