ArticleBMC molecular and cell biology2022
An integrative analysis of DNA methylation and transcriptome showed the dysfunction of MAPK pathway was involved in the damage of human chondrocyte induced by T-2 toxin.
Article in BMC molecular and cell biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 10 citations in OpenAlex.
- Development and validation of an 11-CpG methylation signature-based nomogram for predicting prognosis in early-onset breast cancer.Translational cancer research · 2026Article
- T-2 Toxin-Induced Hepatotoxicity in HepG2 Cells Involves the Inflammatory and Nrf2/HO-1 Pathways.Toxins · 2025Article
- Effects of selenium-mediated RUNX2 overexpression and its transcriptome alterations on Chondrocyte injury in Kashin Beck disease.Frontiers in cell and developmental biology · 2025Article
- Hesperetin Attenuates T-2 Toxin-Induced Chondrocyte Injury by Inhibiting the p38 MAPK Signaling Pathway.Nutrients · 2024Article
- Integrated Analysis of DNA Methylation and Gene Expression Profiles in a Rat Model of Osteoarthritis.International journal of molecular sciences · 2024Article
- Inflammation-related pathways involved in damaged articular cartilage of rats exposed to T-2 toxin based on RNA-sequencing analysis.Frontiers in genetics · 2022Article
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11 authors at 2 institutions in 1 country.
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Abstract
backgroundT-2 toxin is thought to induce the growth plate and articular cartilage damage of Kashin-Beck disease (KBD), an endemic osteochondropathy in China. This study aims to explore the potential underlying mechanism of such toxic effects by integrating DNA methylation and gene expression profiles.
methodsIn this study, C28/I2 chondrocytes were treated with T-2 toxin (5 ng/mL) for 24 h and 72 h. Global DNA methylation level of chondrocyte was tested by Enzyme-Linked Immuno Sorbent Assay. Genome-wide DNA methylation and expression profiles were detected using Illumina Infinium HumanMethylation850 BeadChip and RNA-seq technique, respectively. Differentially methylated genes (DMGs) and differentially expressed genes (DEGs) were identified mainly for two stages including 24 h group versus Control group and 72 h group versus 24 h group. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed by Metascape. DMGs and DEGs were further validated by Sequenom MassARRAY system and quantitative real-time polymerase chain reaction.
resultsThe global DNA methylation levels of chondrocytes exposed to T-2 toxin were significantly increased (P < 0.05). For 24 h group versus Control group (24 VS C), 189 DEGs and 590 DMGs were identified, and 4 of them were overlapping. For 72 h group versus 24 h group (72 VS 24), 1671 DEGs and 637 DMGs were identified, and 45 of them were overlapping. The enrichment analysis results of DMGs and DEGs both showed that MAPK was the one of the mainly involved signaling pathways in the regulation of chondrocytes after T-2 toxin exposure (DEGs: P
conclusionsThe findings depicted a landscape of genomic methylation and transcriptome changes of chondrocytes after T-2 toxin exposure and suggested that dysfunction of MAPK pathway may play important roles in the chondrocytes damage induced by T-2 toxin, which could provide new clues for understanding the potential biological mechanism of KBD cartilage damage induced by T-2 toxin.
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