ArticleBioengineered2022
Inhibition of LncRNA-NEAT1 alleviates intestinal epithelial cells (IECs) dysfunction in ulcerative colitis by maintaining the homeostasis of the glucose metabolism through the miR-410-3p-LDHA axis.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- TIGAR regulates intestinal mucus barrier integrity by inhibiting lactylation of G6PD/6PGD in ulcerative colitis.Nature communications · 2026Article
- Ulcerative colitis: signaling pathways, therapeutic targets and interventional strategies.Signal transduction and targeted therapy · 2026Review
- NEAT1 modulates neutrophil functions via glycolysis to restrain mucosal inflammation in ulcerative colitis.Frontiers in immunology · 2026Article
- Expression Alterations and Correlative Analysis of TPH1/hsa-miR-194-5p/NEAT1 and MAOA/hsa-miR-1276/NEAT1 Axes in Pediatric Inflammatory Bowel Disease.International journal of molecular sciences · 2025Article
- Epigenetic Landscapes in Ulcerative Colitis: From Mechanistic Insights to Clinical Translation.ACS omega · 2025Review
- Global research trends in non-coding RNA and intestinal epithelial homeostasis: an integrated bibliometric analysis (2007-2024).Hereditas · 2025Article
- Emerging Role of Long, Non-Coding RNA Nuclear-Enriched Abundant Transcript 1 in Stress- and Immune-Related Diseases.International journal of molecular sciences · 2025Review
- Article
- Disulfidptosis links the pathophysiology of ulcerative colitis and immune infiltration in colon adenocarcinoma.Scientific reports · 2025Article
- Metabolic regulation of the immune system in health and diseases: mechanisms and interventions.Signal transduction and targeted therapy · 2024Review
- Comprehensive analysis of disulfidptosis-related genes reveals the effect of disulfidptosis in ulcerative colitis.Scientific reports · 2024Article
- Article
- The significance of long non-coding RNAs in the pathogenesis, diagnosis and treatment of inflammatory bowel disease.Precision clinical medicine · 2023Review
- Identification of Critical Modules and Biomarkers of Ulcerative Colitis by Using WGCNA.Journal of inflammation research · 2023Article
- LDHA: The Obstacle to T cell responses against tumor.Frontiers in oncology · 2022Review
- Research advancements and perspectives of inflammatory bowel disease: A comprehensive review.Science progressReview
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysfunction of intestinal epithelial cells (IECs) leads to intestinal epithelial barrier damage and critically involves in the pathogenesis and development of ulcerative colitis (UC). Accumulating studies revealed essential functions of non-coding RNAs in UC. LncRNA NEAT1 (long non-coding RNA nuclear paraspeckle assembly transcript 1) is frequently dysregulated in diverse human diseases. Currently, the precise roles of NEAT1 in the dysfunction of IECs during UC remain unclear. We report NEAT1 was significantly upregulated in IECs from UC patients. In addition, microRNA-410-3p was remarkedly suppressed in IECs from UC patients. Silencing NEAT1 effectively ameliorates the LPS-induced IECs dysfunction. Bioinformatical analysis, RNA pull-down and luciferase assays illustrated that NEAT1 sponged miR-410-3p to downregulate its expression in IECs. Interestingly, the glucose metabolism was obviously elevated in IECs from UC compared with normal colon tissues. Furthermore, NEAT1 promoted and miR-410-3p suppressed glucose metabolism of IECs. We identified lactate dehydrogenase A (LDHA), a glucose metabolism key enzyme, was a direct target of miR-410-3p in IECs. Rescue experiments verified that restoration of miR-410-3p in NEAT1-overexpressing IECs successfully overcame the NEAT1-promoted cell death under LPS treatment by targeting LDHA. In summary, these results unveiled new roles and molecular mechanisms for the NEAT1-mediated IECs dysfunction during the ulcerative colitis.
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