MiR-142-3p Attenuates Oxygen Glucose Deprivation/Reoxygenation-Induced Injury by Targeting FBXO3 in Human Neuroblastoma SH-SY5Y Cells

Jin, Li; Ma, Lishan

doi:10.1016/j.wneu.2019.12.064

Cited by 9 publications

(14 citation statements)

References 33 publications

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“…miR-181c can directly target the 3′-untranslated region of TNF- α mRNA, alleviate inflammation in OGD-elicited microglia, and hamper neuron apoptosis mediated by microglia [ 50 ]. Moreover, other miRNAs like miR-26b [ 51 ], miR-455-3p [ 52 ], miR-199a-5p [ 53 ], and miR-142-3p [ 54 ] also partake in hypoxic-ischemic brain injury development. miR-29b-3p can modulate inflammation in diseases like chronic respiratory disease [ 26 ], sepsis-induced myocardial damage [ 27 ], and osteoarthritis [ 28 ], and miR-29b-3p mimics can weaken the anti-inflammatory function of BMSC exosome H19 in BV2 cells stimulated by LPS in the context of neuroinflammatory diseases [ 55 ].…”

Section: Discussionmentioning

confidence: 99%

Chlorogenic Acid Prevents Microglia-Induced Neuronal Apoptosis and Oxidative Stress under Hypoxia-Ischemia Environment by Regulating the MIR497HG/miR-29b-3p/SIRT1 Axis

et al. 2022

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Background. Chlorogenic acid (CGA) is a polyphenolic compound with antioxidant and anti-inflammatory properties. CGA has been shown to improve neuroinflammation. This study is aimed at elucidating the exact mechanism by which CGA reduces neuroinflammation. Methods. Oxygen and glucose deprivation (OGD) was utilized to treat BV2 microglia and HT-22 hippocampal neurons to engineer an in vitro model of hypoxic ischemia reperfusion. The levels of inflammatory factors (IL-1β, IL-6, TNF-α, IL-4, and IL-10) and oxidative stress factors (MDA, SOD, and GSH-PX) in microglia were determined by ELISA kits. The neuron proliferation was assessed by CCK-8 assay, and LDH kit was used to determine LDH release in neurons. The fluorescent dye DCF-DA was employed to measure ROS levels in neurons. Correlation of MIR497HG, miR-29b-3p, and SIRT1/NF-κB in neurons and microglia was determined by qRT-PCR. Expressions of inflammatory proteins (COX2, iNOS), oxidative stress pathways (Nrf2, HO-1), and apoptosis-related proteins (Bcl-2, Bax, caspase3, caspase8, and caspase9) in microglia or neurons were determined by western blot. The interactions between MIR497HG and miR-29b-3p, as well as between miR-29b-3p and SIRT1, were determined by dual luciferase assay and RIP assay. Results. CGA attenuated OGD-mediated inflammation and oxidative stress in microglia and inhibited microglia-mediated neuronal apoptosis. CGA increased the levels of MIR497HG and SIRT1 and suppressed the levels of miR-29b-3p in BV2 and HT-22 cells. MIR497HG knockdown, miR-29b-3p upregulation, and SIRT1 inhibition inhibited CGA-mediated anti-inflammatory and neuronal protective functions. There is a targeting correlation between MIR497HG, miR-29b-3p, and Sirt1. MIR497HG sponges miR-29b-3p to regulate SIRT1 expression in an indirect manner. Conclusion. CGA upregulates MIR497HG to curb miR-29b-3p expression, hence initiating the SIRT1/NF-κB signaling pathway and repressing OGD-elicited inflammation, oxidative stress, and neuron apoptosis.

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Section: Discussionmentioning

confidence: 99%

Chlorogenic Acid Prevents Microglia-Induced Neuronal Apoptosis and Oxidative Stress under Hypoxia-Ischemia Environment by Regulating the MIR497HG/miR-29b-3p/SIRT1 Axis

et al. 2022

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“…Previous studies have demonstrated that miR-142 plays an important role in various tissue I/R injury including liver. For example, Li et al reported that miR-142 may be a potential agent for protection against cerebral I/R injury through downregulation of FBXO3 (Li and Ma, 2020). Wang et al showed that miR-142-3p attenuated myocardial I/R injury by inhibiting the apoptosis of cardiomyocytes and cardiac fibrosis (Wang et al, 2016).…”

Section: Sevo Postconditioning Reverts I/r-induced Downregulation Of Mir-142mentioning

confidence: 99%

“…Given the key roles of miR-142 in the oxidative stress and inflammatory response in various types of diseases (Li and Ma, 2019;Su et al, 2019), we determine to investigate whether Sevo postconditioning exerts its anti-oxidative and antiinflammatory activities through regulating miR-142. As illustrated in Figures 5A,B, low serum levels of MDA concentration and high serum levels of SOD were observed in the Sevo + HIRI group compared with HIRI group.…”

Section: Sevo Postconditioning Exhibits Anti-oxidative and Anti-inflammatory Activities By Regulating Mir-142mentioning

confidence: 99%

Sevoflurane Postconditioning Attenuates Hepatic Ischemia-Reperfusion Injury by Limiting HMGB1/TLR4/NF-κB Pathway via Modulating microRNA-142 in vivo and in vitro

et al. 2021

Front. Pharmacol.

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Preconditioning of sevoflurane (Sevo) has been demonstrated to protect the liver from ischemia/reperfusion (I/R) injury. However, it is unknown whether it has hepatoprotective when given at the onset of reperfusion (postconditioning), a protocol with more clinical impact. The present study aimed to explore the hepatoprotective effects of Sevo postconditioning against hepatic IR injury in vivo and in vitro and the possible mechanisms. Using a mouse model of hepatic I/R, Sevo postconditioning significantly improved hepatic injury after reperfusion, as demonstrated by reduced AST, ALT, and LDH serum levels and reduced histologic damage in liver tissues. Furthermore, Sevo postconditioning could suppress the apoptosis, inhibit oxidative stress and inflammatory response in liver tissue of HIRI mice, as well as improve the survival rate of HIRI mice. Through analyzing GSE72314 from the gene expression omnibus (GEO) database, it was demonstrated that microRNA (miR)-142 is downregulated by HIRI, which was reversed by Sevo treatment. Further investigation showed that agomiR-142 injection could enhance the hepatoprotective effects of Sevo postconditioning on I/R injury, while antagomiR-142 reversed these effects in mice. Notably, high mobility group box 1 (HMGB1), an important inflammatory factor, was directly targeted by miR-142 in hepatic cells, and we further found that Sevo could inhibit the expression of HMGB1 through up-regulating miR-142 expression in HIRI mice model. In addition, we found that I/R injury induced the activation of TLR4/NF-κB inflammatory pathway was partially suppressed by Sevo postconditioning, and miR-142 mediated the regulatory role of Sevo postconditioning. In line with the in vivo results, Sevo treatment improved the cell viability, inhibited cell apoptosis, oxidative stress and inflammatory response in vitro HIRI model, while these effects were reversed by antagomiR-142 transfection. Collectively, our findings demonstrated that Sevo postconditioning counteracts the downregulation of miR-142 provoked by I/R, in turn decreased the expression of HMGB1, blocking TLR4/NF-κB pathway activation, thus improving hepatic I/R injury. Our data suggest that Sevo may be a valuable alternative anaesthetic agent in liver transplantation and major liver surgeries.

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“…Oxygen glucose deprivation/re-oxygenation (OGD/R) model is often used for ischemia studies via oxygen and glucose deprivation and then reoxygenation to mimic ischemia/reperfusion injury condition. In the OGD/R model, miR-142-3p directly targets FBXO3 to ameliorate inflammation and apoptosis in SH-SY5Y cells ( Li and Ma, 2020 ). The inflammasome is a complex composed of multiple proteins that regulate the maturation and release of pro-inflammatory cytokines, such as IL-1β and IL-18.…”

Section: Introductionmentioning

confidence: 99%

“…The levels of some miRNAs have been shown to correlate with various cancers through negatively regulating genes including F-box proteins ( Lin et al, 2019 ). Analyses using the TargetScan online computational algorithm ( www.targetscan.org ) and luciferase reporter genes showed that FBXO3 is identified as a target of miR-142-3p ( Li and Ma, 2020 ). It has been shown that miR-142-3p plays key roles in tumorigenesis and cancer progression and is expressed at lower levels in breast tumor tissues than in those from normal individuals ( Xu et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Diverse Roles of F-BoxProtein3 in Regulation of Various Cellular Functions

Zhang

Bao

Gao

et al. 2022

Front. Cell Dev. Biol.

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Accumulated evidence shows that the F-box protein 3 (FBXO3) has multiple biological functions, including regulation of immune pathologies, neuropathic diseases and antiviral response. In this review article, we focus on the role of FBXO3 in inflammatory disorders and human malignancies. We also describe the substrates of FBXO3, which contribute to inflammatory disorders and cancers. We highlight that the high expression of FBXO3 is frequently observed in rheumatoid arthritis, leukemia, pituitary adenoma, and oral squamous cell carcinoma. Moreover, we discuss the regulation of FBXO3 by both carcinogens and cancer preventive agents. Our review provides a comprehensive understanding of the role of FBXO3 in various biological systems and elucidates how FBXO3 regulates substrate ubiquitination and degradation during various physiological and pathological processes. Therefore, FBXO3 can be a novel target in the treatment of human diseases including carcinomas.

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MiR-142-3p Attenuates Oxygen Glucose Deprivation/Reoxygenation-Induced Injury by Targeting FBXO3 in Human Neuroblastoma SH-SY5Y Cells

Cited by 9 publications

References 33 publications

Chlorogenic Acid Prevents Microglia-Induced Neuronal Apoptosis and Oxidative Stress under Hypoxia-Ischemia Environment by Regulating the MIR497HG/miR-29b-3p/SIRT1 Axis

Chlorogenic Acid Prevents Microglia-Induced Neuronal Apoptosis and Oxidative Stress under Hypoxia-Ischemia Environment by Regulating the MIR497HG/miR-29b-3p/SIRT1 Axis

Sevoflurane Postconditioning Attenuates Hepatic Ischemia-Reperfusion Injury by Limiting HMGB1/TLR4/NF-κB Pathway via Modulating microRNA-142 in vivo and in vitro

Diverse Roles of F-BoxProtein3 in Regulation of Various Cellular Functions

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