<scp>DJ</scp>‐1 plays a neuroprotective role in <scp>SH‐SY5Y</scp> cells by modulating Nrf2 signaling in response to lidocaine‐mediated oxidative stress and apoptosis

Xue, Ying; Wang, Aizhong

doi:10.1002/kjm2.12218

Cited by 13 publications

(8 citation statements)

References 31 publications

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“…A previous study confirmed that targeting the Keap1/Nrf2 pathway could evidently relieve oxidative stress ( 27 ). Furthermore, it is commonly known that ROS play a crucial role in the activation of numerous biological pathways, and are closely associated with cell proliferation, apoptosis and differentiation ( 28 ).…”

Section: Discussionsupporting

confidence: 55%

Long non‑coding RNA XIST inhibits osteoblast differentiation and promotes osteoporosis via Nrf2 hyperactivation by targeting CUL3

Chen

Zhai

et al. 2021

Int J Mol Med

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Osteoporosis (OP) is a common skeletal disorder characterized by a low bone mass and the deterioration of bone structure. Long non-coding (lnc)RNA X inactive-specific transcript (XIST) is highly expressed in the serum and monocytes of patients with OP. Thus, the purpose of the present study was to explore the mechanisms underlying the role of XIST in the progression of OP. To establish animal models of OP, female rats underwent a bilateral ovariectomy. The bone mineral density of individual rats was measured using dual-energy X-ray absorptiometry. The combination of XIST and cullin-3 (CUL3) was analyzed using a dual-luciferase reporter assay. Bone histopathological changes were assessed by hematoxylin and eosin staining. Alkaline phosphatase activity was examined by ALP staining. Finally, a series of functional experiments were performed to examine the effects of XIST on cellular behaviors. In the present study, XIST promoted OP and inhibited bone formation by regulating the expression levels of CUL3 and nuclear factor erythroid 2-related factor 2 (Nrf2) in the rats with OP. Moreover, XIST directly targeted CUL3 and negatively regulated its expression. Of note, CUL3 downregulation reversed the effects of XIST silencing on cell viability, differentiation and mineralization, as well as the expression of Nrf2 and CUL3 in MC3T3-E1 cells. Collectively, XIST was demonstrated to inhibit the differentiation of osteoblasts and promote OP by inhibiting the degradation of Nrf2 via targeting CUL3.

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Section: Discussionsupporting

confidence: 55%

Long non‑coding RNA XIST inhibits osteoblast differentiation and promotes osteoporosis via Nrf2 hyperactivation by targeting CUL3

Chen

Zhai

et al. 2021

Int J Mol Med

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“…Lidocaine has been reported to substantially reduce cell viability in a concentrationdependent manner, though low concentrations ( 1 mM) have not been found to cause significant cytotoxicity. [16][17][18] In the present study, the MTT assay revealed no distinct cytotoxicity at lidocaine concentrations 1 mM. This result was considered in subsequent real-time RT-PCR and western blotting experiments, wherein 0.5 mM lidocaine was investigated, in order to avoid adverse effects on HDPSC survival.…”

Section: Discussionmentioning

confidence: 75%

Lidocaine inhibits osteogenic differentiation of human dental pulp stem cells in vitro

et al. 2023

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Objective Lidocaine is an amide local anaesthetic commonly used for pain control, however, few studies have investigated the effect of lidocaine on the osteogenic differentiation of human dental pulp stem cells (HDPSCs). The present study aimed to determine the effect of lidocaine on HDPSC viability and osteogenic differentiation. Methods HDPSCs were incubated with 0, 0.05, 0.2, 0.5, and 1 mM lidocaine for 24, 48 and 72 h, after which, MTT assays were performed. HDPSCs cultured with the above lidocaine concentrations and osteogenic differentiation medium for 7 and 14 days were stained for alkaline phosphatase (ALP). Protein and mRNA levels of relevant osteogenic factors (bone morphogenetic protein-2 [BMP-2] and runt-related transcription factor 2 [RUNX2]) were examined using western blotting and real-time reverse-transcription polymerase chain reaction, respectively. Results Lidocaine did not affect the viability of HDPSCs, however, lidocaine reduced ALP activity in HDPSCs. Levels of ALP, BMP-2, and RUNX2 mRNA were reduced with lidocaine, and levels of BMP-2 and RUNX2 proteins were decreased, versus controls. Conclusions Lidocaine inhibits osteogenic differentiation markers in HDPSCs in vitro, even at low concentrations, without cytotoxicity. This study suggests that lidocaine may inhibit osteogenic differentiation in HDPSC-mediated regenerative medicine, including pulp regeneration and repair.

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“…It was shown that eliminating DJ-1 rendered SH-SY5Y susceptibility to cell death [72]. DJ-1 was confirmed to inhibit oxidative stress and consequently leads to cell protection [73,74]. As a fast-reacting oxidation sensor, the degree of its oxidized form (on Cys106) [75] is a proxy for a cell's oxidative status.…”

Section: Discussionmentioning

confidence: 99%

Alteration in Long Noncoding RNAs in Response to Oxidative Stress and Ladostigil in SH-SY5Y Cells

Zohar¹,

Giladi²,

Eliyahu³

et al. 2022

Preprint

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Microglia activation causes neuroinflammation, which is a hallmark of neurodegenerative disorders, brain injury, and aging. Ladostigil, a bifunctional reagent with antioxidant and anti-inflammatory properties, reduced microglial activation and enhanced brain functioning in elderly rats. In this study, we studied SH-SY5Y, a human neuroblastoma cell line, and tested viability in the presence of hydrogen peroxide and Sin1 (3-morpholinosydnonimine), which generates reactive oxygen and nitrogen species (ROS/RNS). Both stressors caused significant apoptosis and necrotic cell death that was attenuated by ladostigil. Our results from RNA-seq experiments show that long non-coding RNAs (lncRNAs) account for 30% of all transcripts in SH-SY5Y cells treated with Sin1 for 24 hours. Altogether, we identify 94 differently expressed lncRNAs in the presence of Sin1, including MALAT1, a highly expressed lncRNA with anti-inflammatory and anti-apoptotic functions. Additional activities of Sin-1 upregulated lncRNAs include redox homeostasis (e.g., MIAT, GABPB1-AS1), energy metabolism (HAND2-AS1), and neurodegeneration (e.g., MIAT, GABPB1-AS1, NEAT1). Four lncRNAs implicated as enhancers were significantly upregulated in cells exposed to Sin1 and ladostigil. Finally, we show that H2O2 and Sin1 increased the expression of DJ-1, a redox sensor and modulator of Nrf2 (nuclear factor erythroid 2–related factor 2). Nrf2 (NFE2L2 gene) is a major transcription factor regulating antioxidant genes. In the presence of ladostigil, DJ-1 expression is restored to its baseline. The mechanisms governing SH-SY5Y cell survival and homeostasis are highlighted by the beneficial role of ladostigil in the crosstalk involving Nrf2, antioxidant transcription factor DJ-1, and lncRNAs. Stress-dependent induction of lncRNAs represents an underappreciated regulatory level that contributes to cellular homeostasis and the capacity of SH-SY5Y to cope with oxidative stress.

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DJ‐1 plays a neuroprotective role in SH‐SY5Y cells by modulating Nrf2 signaling in response to lidocaine‐mediated oxidative stress and apoptosis

Cited by 13 publications

References 31 publications

Long non‑coding RNA XIST inhibits osteoblast differentiation and promotes osteoporosis via Nrf2 hyperactivation by targeting CUL3

Long non‑coding RNA XIST inhibits osteoblast differentiation and promotes osteoporosis via Nrf2 hyperactivation by targeting CUL3

Lidocaine inhibits osteogenic differentiation of human dental pulp stem cells in vitro

Alteration in Long Noncoding RNAs in Response to Oxidative Stress and Ladostigil in SH-SY5Y Cells

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