ArticleAmerican journal of translational research2020
Overexpression of lncRNA Gm43050 alleviates apoptosis and inflammation response induced by sevoflurane treatment by regulating miR-640/ZFP91.
Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- lncRNA PART1 improves sevoflurane-induced impairments in learning and cognitive function by regulating miR-16-5p expression and reducing neuroinflammation.Toxicology research · 2025Article
- Effects of lncRNA HOXA11-AS on Sevoflurane-Induced Neuronal Apoptosis and Inflammatory Responses by Regulating miR-98-5p/EphA4.Mediators of inflammation · 2023Article
- Sevoflurane reverses cisplatin resistance in neuroblastoma cells through the linc00473/miR-490-5p/AKT1 axis.Saudi medical journal · 2022Article
- Sevoflurane anesthesia ameliorates LPS-induced acute lung injury (ALI) by modulating a novel LncRNA LINC00839/miR-223/NLRP3 axis.BMC pulmonary medicine · 2022Article
- ZFP91 promotes cell proliferation and inhibits cell apoptosis in AML via inhibiting the proteasome-dependent degradation of RIP1.International journal of medical sciences · 2022Article
- Sevoflurane induces inflammation in primary hippocampal neurons by regulating Hoxa5/Gm5106/miR-27b-3p positive feedback loop.Bioengineered · 2021Article
- The Role of miR-640: A Potential Suppressor in Breast CancerFrontiers in oncology · 2021Article
- Full-Length Transcriptome Sequencing: An Insight Into the Dog Model of Heart Failure.Frontiers in cardiovascular medicine · 2021Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsThe present study investigated the function and mechanism of lncRNA Gm43050 in sevoflurane-induced abnormal cognition.
methodsPrimary hippocampal neurons were used to establish the model of abnormal cognitive disorder. Overexpression and knockdown experiments were performed to analyze cell death rates, proliferation, apoptosis and the inflammatory response. The dual-luciferase reporter assay was used to analyze the potential binding targets of lncRNA Gm43050. Rescue experiments were used to assess the downstream targets of Gm43050.
resultsWe found that lncRNA Gm43050 was in the cytoplasm. Overexpression of lncRNA Gm43050 had no impact on proliferation but significantly reduced the cell death rates and apoptosis. The inflammation markers IL-6, IL-1β, IL-8 and TNF-α were manifestly downregulated in the overexpression group. Opposite effects were detected in the lncRNA Gm43050 knockdown group. Bioinformatics analysis showed that miR-640 may be the potential target of Gm43050. Additionally, we found that ZFP91 was the downstream target of miR-640.
conclusionWe provided comprehensive data of the function and mechanism of lncRNA Gm43050 in abnormal cognition. Our study showed that lncRNA Gm43050 exerted its important role via the regulation of miR-640 and ZFP91.
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Identifiers
32913509PMC7476152What OpenQuestion holds
Registered trials
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