Skip to main content
. 2018 Jul 6;50(7):1–9. doi: 10.1038/s12276-018-0114-1

Fig. 4. CSE-induced upregulation of PAR2 is dependent on p38 activation.

Fig. 4

a BEAS-2B cells were treated with CSE (1%) for the indicated times. Total cellular extracts were subjected to western blot analysis for p-ERK, p-p38, p-Akt, and GAPDH. b Cells were pre-treated with an MEK inhibitor (U0126, 2 or 10 μM), PI3K/Akt inhibitor (LY294002, 10 μM), or p38 inhibitor (SB203580, 10 μM) for 2 h and then stimulated with CSE for 24 h in the presence of U0126, LY294002, or SB203580. Membrane and cytoplasmic proteins were extracted and subjected to western blot analysis for PAR2 and heat shock protein 90 (Hsp90). c BEAS-2B cells were pre-treated with SB203580 (10 μM) for 2 h and then stimulated with CSE (1%) in the presence or absence of SB203580 for 24 h. The cells were stimulated with VC or NE (1 U/ml) for 24 h in the absence of SB203580 and CSE. IL-8 concentrations in cell supernatants were measured by multiplex bead assay. Data represent the mean ± SD; **P < 0.05