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RESEARCH ARTICLE
Year : 2022  |  Volume : 17  |  Issue : 6  |  Page : 1357-1363

Schwann cells differentiated from skin-derived precursors provide neuroprotection via autophagy inhibition in a cellular model of Parkinson’s disease


1 Department of Neurology, Affiliated Hospital of Nantong University; Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, China
2 Department of Clinical Medicine, The First Clinical Medical College of Xuzhou Medical University, Xuzhou, Jiangsu Province, China
3 Department of Neurology, Affiliated Hospital of Nantong University, Nantong; Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, The Second Afflicted Hospital of Soochow University, Suzhou, Jiangsu Province, China
4 Department of Neurology, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, China

Correspondence Address:
Kai-Fu Ke
Department of Neurology, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province
China
Xiao-Su Gu
Department of Neurology, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province
China
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Source of Support: This study was supported by Technology Project of Nantong of China, Nos. JC2020052 (to XSG), JCZ19087 (to XSG); and the National Natural Science Foundation of China, Nos. 81873742 (to KFK), 81901195 (to JBS), 81502867 (to TX), 82073627 (to TX), Conflict of Interest: None


DOI: 10.4103/1673-5374.327353

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Autophagy has been shown to play an important role in Parkinson’s disease. We hypothesized that skin-derived precursor cells exhibit neuroprotective effects in Parkinson’s disease through affecting autophagy. In this study, 6-hydroxydopamine-damaged SH-SY5Y cells were pretreated with a culture medium containing skin-derived precursors differentiated into Schwann cells (SKP-SCs). The results showed that the SKP-SC culture medium remarkably enhanced the activity of SH-SY5Y cells damaged by 6-hydroxydopamine, reduced excessive autophagy, increased tyrosine hydroxylase expression, reduced α-synuclein expression, reduced the autophagosome number, and activated the PI3K/AKT/mTOR pathway. Autophagy activator rapamycin inhibited the effects of SKP-SCs, and autophagy inhibitor 3-methyladenine had the opposite effect. These findings confirm that SKP-SCs modulate the PI3K/AKT/mTOR pathway to inhibit autophagy, thereby exhibiting a neuroprotective effect in a cellular model of Parkinson’s disease. This study was approved by the Animal Ethics Committee of Laboratory Animal Center of Nantong University (approval No. S20181009-205) on October 9, 2018.


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