IGF - IGF-1 inhibits MPTP/MPP+-induced autophagy on dopaminergic neurons through the

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Related Articles IGF-1 inhibits MPTP/MPP+-induced autophagy on dopaminergic neurons through the IGF-1R/PI3k-Akt-mTOR pathway and GPER.

Am J Physiol Endocrinol Metab. 2020 Aug 31;:

Authors: Wang XW, Yuan LJ, Yang Y, Zhang M, Chen WF

Abstract
Autophagy dysfunctions are involved in the pathogenesis of Parkinson disease (PD). In the present study, we aimed to evaluate the involvement of G-protein coupled estrogen receptor (GPER) in the inhibitory effect of insulin-like growth factor-1 (IGF-1) against excessive autophagy in PD animal and cellular models. 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) treatment significantly induced mice movement disorder and decreased the protein level of tyrosine hydroxylase (TH) in the substantia nigra (SN) and dopamine (DA) content in striatum. Along with the dopamine neuron injury, we observed significant up-regulations of microtubule associated light chain-3 II (LC3-II) and ?-synuclein as well as a down-regulation of P62 in MPTP-treated mice. These changes could be restored by IGF-1 pretreatment. Co-treatment with IGF-1R antagonist JB-1 or GPER antagonist G15 could block the neuroprotective effects of IGF-1. 1-methy-4-phenylpyridinium (MPP+) treatment could also excessively activate autophagy along with the reduction of cell viability in SH-SY5Y cells. IGF-1 could inhibit the neurotoxicity through promoting the phosphorylation of Akt and mTOR, which could also be antagonized by JB-1 or G15. These data suggest that IGF-1 inhibits MPTP/MPP+-induced autophagy on dopaminergic neurons through the IGF-1R/PI3k-Akt-mTOR pathway and GPER.


PMID: 32865008 [PubMed - as supplied by publisher]



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Insulin like growth factors
IGF-1
Igf-1r3

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