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. 2016 May 23;6:26547. doi: 10.1038/srep26547

Figure 2. Signaling pathways mediating the effect of fetal NP cell proliferation promoting compounds.

Figure 2

(A) None of the chemicals significantly promoted Erk1/2 phosphorylation. ERKi U0126 as expected downregulated Erk1/2 phosphorylation. (B) Co-administration of U0126 markedly increased the effect of GSK3i BIO but had no effect on the other chemicals. Mean ± s.d., n = 4. (C) Short-term (15 minutes) U0126 treatment led to a marked increase in Akt phosphorylation at both S473 and T308. Increase in Akt phosphorylation was also detected in cells treated with A1/A3 adenosine receptor agonists CPA and β-adrenoceptor agonist NE. (D) The effect of U0126 on Akt phosphorylation was significantly inhibited by Akt inhibitors Deguelin (20 nM) or Tricirbine (500 nM). (E) The effect of U0126 on the fetal NP cell proliferation was also significantly inhibited by Deguelin or Tricirbine. Mean ± s.d., n = 4. (F) PMA (1 μM) promoted Erk1/2 phosphorylation but inhibited Akt phosphorylation in fetal NP cells. (G) PMA adversely regulated fetal NP cell proliferation. Mean ± s.d., n = 4. *P < 0.05. **P < 0.01. All gels were run under the same experimental condition. Cropped images were shown in the figure. Full length blots are included in the Supplementary Information.