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The aim of this study was to further confirm that glial cell line-derivedneurotrophic factor (GDNF) exerts a neuro-protective effect on dopaminergic neurons(DAs) and to investigate the protective mechanism. Cadherins are calcium-dependentadhesion proteins, and N-cadherins are found in neurons. Our study attempted toascertain whether GDNF activates the PI3K/Akt signaling pathway through the mediationof N-cadherin to confer a protective effect on DAs. Flow cytometry and Hoechst 33258staining results indicated that the apoptosis rate of damaged neurocytes increasedfollowing interference of N-cadherin expression. Immunoblotting results demonstratedthat the amount of phosphorylated Akt (p-Akt) in the cytoplasm decreased, whilethe total Akt quantity remained unchanged following interference of N-cadherinexpression. The immunohistochemical staining results demonstrated that the levelsof total N-cadherin, phosphorylated N-cadherin (Tyr860) and p-Akt decreased; however,the amount of total Akt remained unchanged. In addition, we also demonstratedthat Tyr860 and p-Akt levels were reduced in a GDNF dose-dependent manner withthe phosphorylation level peaking at GDNF dose of 50 ng/ml (in vitro) and 50 ng/4 µl(in vivo), and also in a time-dependent manner with the phosphorylation levelpeaking at 15 min (in vitro) and 30 min (in vivo). Statistical analysis also showedthat changes in the phosphorylation levels of Tyr860 and p-Akt demonstrated apositive correlation. Collectively, GDNF activates the PI3K/Akt pathway via N-cadherinto protect DAs.

Involvement of N-cadherin in the protective effect of glial cell line-derived neurotrophic factor on dopaminergic neuron damage