Background: High glucose (HG) is linked to dopaminergic neuron loss and related Parkinson’s disease (PD), but the mechanism is unclear. Results: Rats and differentiated SH-SY5Y cells were used to investigate the effect of HG on dopaminergic neuronal apoptotic death. We found that a 40-day HG diet elevated cleaved caspase 3 levels and activated Fyn and mTOR/S6K signaling in the substantia nigra of rats. In vitro, 6 days of HG treatment activated Fyn, enhanced binding between Fyn and mTOR, activated mTOR/S6K signaling, and induced neuronal apoptotic death. The proapoptotic effect of HG was rescued by either the Fyn inhibitor PP1 or the mTOR inhibitor rapamycin. PP1 inhibited mTOR/S6K signaling, but rapamycin was unable to modulate Fyn activation. Conclusions: HG induces dopaminergic neuronal apoptotic death via the Fyn/mTOR/S6K pathway.
CITATION STYLE
Tan, C., Liu, X., Zhang, X., Peng, W., Wang, H., Zhou, W., … Chen, L. (2021). Fyn kinase regulates dopaminergic neuronal apoptosis in animal and cell models of high glucose (HG) treatment. BMC Molecular and Cell Biology, 22(1). https://doi.org/10.1186/s12860-021-00398-y
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