ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2023
The potential role of N6-methyladenosine modification of LncRNAs in contributing to the pathogenesis of chronic glomerulonephritis.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- m6A Ribonucleic Acid Methylation in Fibrotic Diseases of Visceral Organs.Small science · 2025Review
- The role of N6-methyladenosine (mPeerJ · 2025Review
- Role of mZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Review
- Methyltransferase-like 3 represents a prospective target for the diagnosis and treatment of kidney diseases.Human genomics · 2024Review
- The role of N-methyladenosine modification in acute and chronic kidney diseases.Molecular medicine (Cambridge, Mass.) · 2023Review
- Identification of Rab7 as an autophagy marker: potential therapeutic approaches and the effect of Qi Teng Xiao Zhuo granule in chronic glomerulonephritis.Pharmaceutical biology · 2023Article
- N6-methyladenosine methylation in kidney injury.Clinical epigenetics · 2023Review
- Understanding the interplay between N6-methyladenine RNA methylation and noncoding RNAs in kidney disease.Clinical and translational discovery · 2023Article
- Construction of chronic glomerulonephritis‑related lncRNA‑mRNA regulatory network and lncRNA‑-miRNA‑mRNA ceRNA network by bioinformatics analysis.Experimental and therapeutic medicine · 2023Article
- Overexpression of FTO inhibits excessive proliferation and promotes the apoptosis of human glomerular mesangial cells by alleviating FOXO6 m6A modification via YTHDF3-dependent mechanisms.Frontiers in pharmacology · 2023Article
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5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundIncreasing evidence indicates that N6-methyladenosine (m6A) modification of mRNAs has been shown to play a critical role in the occurrence and development of many diseases, while little is known about m6A modification in long non-coding RNAs (LncRNAs). Our study aims to investigate the potential functions of LncRNA m6A modifications in lipopolysaccharide (LPS)-induced mouse mesangial cells (MMCs), providing us with a new perspective on the molecular mechanisms of chronic glomerulonephritis (CGN) pathogenesis.
methodsDifferentially methylated LncRNAs were identified by Methylated RNA immunoprecipitation sequencing (MeRIP-seq). LncRNA-mRNA and LncRNA-associated LncRNA-miRNA-mRNA (CeRNA) networks were constructed by bioinformatics analysis. Furthermore, we utilized gene ontology (GO) and pathway enrichment analyses (KEGG) to explore target genes from co-expression networks. In addition, the total level of m6A RNA methylation and expression of methyltransferase and pro-inflammatory cytokines were detected by the colorimetric quantification method and western blot, respectively. Cell viability and cell cycle stage were detected by cell counting kit-8 (CCK-8) and flow cytometry.
resultsIn total, 1141 differentially m6A-methylated LncRNAs, including 529 hypermethylated LncRNAs and 612 hypomethylated LncRNAs, were determined by MeRIP-seq. The results of GO and KEGG analysis revealed that the target mRNAs were mainly enriched in signal pathways, such as the NF-kappa B signaling pathway, MAPK signaling pathway, Toll-like receptor signaling pathway, and apoptosis signaling pathway. In addition, higher METTL3 expression was found in CGN kidney tissues using the GEO database. METTL3 knockdown in MMC cells drastically reduced the levels of m6A RNA methylation, pro-inflammatory cytokines IL6 and TNF-α, and inhibited cell proliferation and cycle progression.
conclusionsOur findings provide a basis and novel insight for further investigations of m6A modifications in LncRNAs for the pathogenesis of CGN.
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