Silencing long noncoding RNA-CES1P1 suppresses glomerular endothelial cell inflammation in diabetic nephropathy

Zhang, Xiaona; Ren, Long; Wei, Jiaxing; Ni, Yanan; Sun, Lulu; Zhao, Xiaoyu; Zhang, Yaguang; Qiao, Hong

doi:10.1016/j.intimp.2022.108820

Cited by 3 publications

(2 citation statements)

References 34 publications

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“…MAG (myelin associated glycoprotein) [52] participate in pathogenic processes of Parkinson’s disease. Recent evidence indicates that BCAS1 [46], MAG (myelin associated glycoprotein) [49] and CES1P1 [53] are key to progression of inflammation. Previous research suggested some cardiac biomarkers, such as ZNF208 [54] and PEG3 [55] could be valuable in the diagnosis and prognosis of cardiovascular diseases.…”

Section: Discussionmentioning

confidence: 99%

Identification of key genes and signaling pathway in the pathogenesis of Huntington's disease via bioinformatics and next generation sequencing data analysis

Vastrad,

Vastrad

2024

Preprint

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Huntington's disease (HD) is the primary cause of progressive motor deficits, psychiatric symptoms, and cognitive impairment. The exact molecular mechanisms of HD pathogenesis are largely unknown. This investigation aims to identify the hub genes, miRNA and TFs in HD and explore their potential molecular regulatory network. Next generation sequencing (NGS) dataset (GSE105041) was extracted from the Gene Expression Omnibus (GEO) database. An integrated bioinformatics pipeline including identification of differentially expressed genes (DEGs), Gene ontology and REACTOME pathway enrichment analysis, protein-protein interaction (PPI) network and module analysis, miRNA-hub gene regulatory network analysis and TF-hub gene regulatory network analysis, and receiver operating characteristic curve (ROC) analysis were applied to identify hub genes, miRNA and TFs, and key drivers of HD pathogenesis. We identified 958 DEGs in the discovery phase, consisting of 479 up regulated genes and 479 down regulated genes. GO and REACTOME enrichment analyses of the 479 up regulated genes and 479 down regulated genes showed that they were mainly involved in multicellular organismal process, developmental process, signaling by GPCR and MHC class II antigen presentation. Further analysis of the PPI network using Cytoscape and PEWCC plugins identified 10 hub genes, including LRRK2, MTUS2, HOXA1, IL7R, ERBB3, EGFR, TEX101, WDR76, NEDD4L and COMT. Possible target miRNAs and TFs, including hsa-mir-1292-5p, hsa-mir-4521, ESRRB and SREBF1, were predicted by constructing a miRNA-hub gene regulatory network analysis and TF-hub gene regulatory network. This investigation used bioinformatics methods to explore the molecular pathogenesis of HD, and identified potential molecular markers. These molecular markers might provide novel ideas and methods for the early diagnosis, treatment, and monitoring of HD.

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Section: Discussionmentioning

confidence: 99%

Identification of key genes and signaling pathway in the pathogenesis of Huntington's disease via bioinformatics and next generation sequencing data analysis

Vastrad,

Vastrad

2024

Preprint

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“…MiR-214-3p reportedly promotes kidney injury and inflammatory responses in hyperlipidemic pancreatitis [ 18 ]. Moreover, miR-214-3p promotes renal inflammatory infiltration in diabetic nephropathy [ 34 ]. These data support our results that miR-214-3p acts as a pivotal regulator in the pathogenesis of sepsis-induced AKI.…”

Section: Discussionmentioning

confidence: 99%

CircRNA itchy E3 ubiquitin protein ligase improves mitochondrial dysfunction in sepsis-induced acute kidney injury by targeting microRNA-214-3p/ATP-binding cassette A1 axis

Ye,

Miao,

et al. 2023

Renal Failure

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Background Circular RNAs (circRNAs) are promising biomarkers and therapeutic targets for acute kidney injury (AKI). In this study, we investigated the mechanism by which circRNA itchy E3 ubiquitin protein ligase (circ-ITCH) regulates sepsis-induced AKI. Methods A sepsis-induced AKI mouse model was created using LPS induction and circ-ITCH overexpression. Circ-ITCH levels were confirmed via RT-qPCR. Kidney tissue changes were examined through various stains and TUNEL. Enzyme-linked immunosorbent assay (ELISA) gauged oxidative stress and inflammation. Mitochondrial features were studied with electron microscopy. RT-qPCR and western blotting assessed mitochondrial function parameters. Using starBase, binding sites between circ-ITCH and miR-214-3p, as well as miR-214-3p and ABCA1, were predicted. Regulatory connections were proven by dual-luciferase assay, RT-qPCR, and western blotting. Results Circ-ITCH expression was downregulated in LPS-induced sepsis mice. Overexpression of circ-ITCH ameliorates indicators of renal function (serum creatinine [SCr], blood urea nitrogen [BUN], neutrophil gelatinase-associated lipocalin [NGAL], and kidney injury molecule-1 [Kim-1]), reduces renal cell apoptosis, mitigates oxidative stress markers (reactive oxygen species [ROS] and malondialdehyde [MDA]), and diminishes inflammatory markers (interleukin [IL]-1β, IL-6, and tumor necrosis factor [TNF-α]). Moreover, circ-ITCH overexpression alleviated mitochondrial damage and dysfunction. Furthermore, circ-ITCH acts as a sponge for miR-214-3p, thereby upregulating ABCA1 expression. In addition, the miR-214-3p inhibitor repressed oxidative stress, inflammation, and mitochondrial dysfunction, which was reversed by circ-ITCH knockdown. Further cellular analysis in HK-2 cells supported these findings, highlighting the protective role of circ-ITCH against sepsis-induced AKI, particularly through the miR-214-3p/ABCA1 axis. Conclusion The novel circ-ITCH/miR-214-3p/ABCA1 pathway plays an essential role in the regulation of oxidative stress and mitochondrial dysfunction in sepsis-induced AKI.

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A systematic review of epigenetic interplay in kidney diseases: Crosstalk between long noncoding RNAs and methylation, acetylation of chromatin and histone

Tan,

Jia,

et al. 2024

Biomedicine & Pharmacotherapy

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Silencing long noncoding RNA-CES1P1 suppresses glomerular endothelial cell inflammation in diabetic nephropathy

Cited by 3 publications

References 34 publications

Identification of key genes and signaling pathway in the pathogenesis of Huntington's disease via bioinformatics and next generation sequencing data analysis

Identification of key genes and signaling pathway in the pathogenesis of Huntington's disease via bioinformatics and next generation sequencing data analysis

CircRNA itchy E3 ubiquitin protein ligase improves mitochondrial dysfunction in sepsis-induced acute kidney injury by targeting microRNA-214-3p/ATP-binding cassette A1 axis

A systematic review of epigenetic interplay in kidney diseases: Crosstalk between long noncoding RNAs and methylation, acetylation of chromatin and histone

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