Inhibition of glycogen synthase kinase-3β reduces ROS production and alters antioxidant enzyme activities in MPP+-induced neuronal cell death

Armağan, Güliz; Sevgili, Elvin; Bilgiç, Tuğçe; Gürkan, Fulya Tuzcu; Dağcı, Taner

doi:10.1016/j.freeradbiomed.2017.04.140

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“…29 GSK3β knockdown resulted in a decrease in ROS production and MPP + -induced cell death in the SH-SY5Y cells. 30 Overexpression of GSK3β inhibited autophagy and induced the augmentation of α-syn in the PC12 cells. 31 Moreover, GSK3β dysregulation led to deterioration of the SN and the phosphorylation and accumulation of tau and α-syn.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, several lines of evidence have indicated that knockdown of GSK3β protected dopaminergic neurons from MPTP neurotoxicity . GSK3β knockdown resulted in a decrease in ROS production and MPP + ‐induced cell death in the SH‐SY5Y cells . Overexpression of GSK3β inhibited autophagy and induced the augmentation of α‐syn in the PC12 cells .…”

Section: Discussionmentioning

confidence: 99%

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Upregulated lncRNA small nucleolar RNA host gene 1 promotes 1‐methyl‐4‐phenylpyridinium ion‐induced cytotoxicity and reactive oxygen species production through miR‐15b‐5p/GSK3β axis in human dopaminergic SH‐SY5Y cells

Xie

et al. 2018

J of Cellular Biochemistry

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Long noncoding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) has been demonstrated to be upregulated and play a crucial role in the pathology of Parkinson's disease (PD). However, the exact role of SNHG1 and its underlying mechanisms in PD remains elusive. In this study, we found that SNHG1 and glycogen synthase kinase 3 beta (GSK3β) were upregulated, but miR‐15b‐5p was downregulated in 1‐methyl‐4‐phenylpyridinium ion (MPP+)‐treated SH‐SY5Y cells. The upregulation of SNHG1 enhanced MPP+‐induced cellular toxicity in SH‐SY5Y cells, as shown by decreased cell viability, increased ROS production, and increased number of TdT‐mediated dUTP Nick‐End labeling‐positive cells, accompanied with the upregulation of cleaved caspase 3 and elevation of cytochrome C release. Meanwhile, SNHG1 knockdown presented the converse effects. SNHG1 was demonstrated to interact with miR‐15b‐5p. Moreover, SNHG1 could attenuate the inhibitory effects of miR‐15b‐5p on MPP+‐induced cytotoxicity and production of ROS. Besides, GSK3β was identified as a direct target of miR‐15b‐5p. The inhibitory effects of SNHG1 knockdown or miR‐15b‐5p overexpression on MPP+‐induced cytotoxicity and reactive oxygen species (ROS) production were abrogated by upregulation of GSK3β. Taken together, these results demonstrate that upregulated lncRNA SNHG1 promotes MPP+‐induced cytotoxicity and ROS production through the miR‐15b‐5p/GSK3β axis in human dopaminergic SH‐SY5Y cells, suggesting that SNHG1 may act as a potential therapeutic target for PD treatment in the future.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%