图5.

神经生长因子可能通过激活pERK/MASH1信号通路诱导肾上腺髓质嗜铬细胞发生神经元转分化(n=5)

Figure 5 NGF-induced neuron transition of AMCCs by activation of pERK/MASH1 signaling pathway (n=5)

A and B: A rise in neurite elongation by NGF interference is attenuated substantially after exposure to PD98059. C and D: After exposure to NGF, the protein levels of pERK, and protein as well as mRNA levels of JMJD3 and MASH1 in AMCCs are significantly elevated, which is reversed by the treatment of PD98059. The protein expression of PNMT is upregulated and the level of peripherin is downregulated by PD98059 treatment. E: The application of DEX to AMCCs inhibits the activation of pERK/MASH1 signaling by NGF treatment. *P<0.05 vs the NGF group, **P<0.01 vs the NGF group, ††P<0.01 vs the PD98059 group. NGF: Nerve growth factor; AMCCs: Adrenal medulla chromaffin cells; PNMT: Phenylethanolamine N-methyl transferase; DEX: Dexamethasone.