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. Author manuscript; available in PMC: 2015 Jul 1.
Published in final edited form as: Pain. 2014 Apr 13;155(7):1328–1338. doi: 10.1016/j.pain.2014.04.009

Fig. 5. PAR2 is involved in ERK signaling and calcium influx.

Fig. 5

(A) Western blot shows DRG (S1–S4) p-ERK1/2 expression at day 30 from mice with EAP (n=3) compared to naive (n=3) and PAR2 deficient mice with EAP (PAR2 KO-EAP; n=3) compared to control (PAR2 KO-Naive; n=3). (B) Densitometry data showed a significant increased in p-ERK1/2 expression in mice (B6) with EAP compared to naive cohorts and (C) no difference in p-ERK1/2 expression was observed between PAR2 KO-Naive and PAR2 KO-EAP. (D) Representative immunofluorescence of p-ERK 1/2 (green) in DRG of mice with EAP and naive at day 30 showed increased p-ERK1/2. (E and G) Changes in [Ca2+]i were recorded before (45 seconds) and after (150 seconds) delivery of 1nm capsaicin to DRG extracted from mice with EAP and compared to naive cohorts. (G) EAP treated animals showed a significant increase in [Ca2+]i compared to control. (F and H) However, [Ca2+]i remained the same in DRG from PAR2 KO-EAP compared to PAR2 KO-Naive at day 30. Calcium experiments were repeated independently at least three times. Scale bars represent 50µm and (*) denotes p<0.05.