ArticleFrontiers in immunology2022
Long Intergenic Noncoding RNA MIAT as a Regulator of Human Th17 Cell Differentiation.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- MIAT: An important long non-coding RNA regulating cardiovascular and cerebrovascular diseases.Frontiers in cardiovascular medicine · 2026Review
- Article
- LINC01013 reverses bisphosphonate-impaired osteogenic differentiation of JBMMSCs by regulating intracellular translocation of ILF3.Stem cell research & therapy · 2025Article
- CXCL13 Damages Blood Spinal Cord Barrier by Promoting RNF6/Sqstm1-Ubiquitination Induced Autophagy in Experimental Allergic Encephalomyelitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Long noncoding RNA LIRIL2R modulates FOXP3 levels and suppressive function of human CD4Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The regulatory relationship between transcription factor STAT3 and noncoding RNA.Cellular & molecular biology letters · 2024Review
- PIM kinases regulate early human Th17 cell differentiation.Cell reports · 2023Article
- RNA circuits and RNA-binding proteins in T cells.Trends in immunology · 2023Review
- Non-coding RNAs in immunoregulation and autoimmunity: Technological advances and critical limitations.Journal of autoimmunity · 2023Review
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
T helper 17 (Th17) cells protect against fungal and bacterial infections and are implicated in autoimmunity. Several long intergenic noncoding RNAs (lincRNA) are induced during Th17 differentiation, however, their contribution to Th17 differentiation is poorly understood. We aimed to characterize the function of the lincRNA Myocardial Infarction Associated Transcript (MIAT) during early human Th17 cell differentiation. We found MIAT to be upregulated early after induction of human Th17 cell differentiation along with an increase in the chromatin accessibility at the gene locus. STAT3, a key regulator of Th17 differentiation, directly bound to the MIAT promoter and induced its expression during the early stages of Th17 cell differentiation. MIAT resides in the nucleus and regulates the expression of several key Th17 genes, including IL17A, IL17F, CCR6 and CXCL13, possibly by altering the chromatin accessibility of key loci, including IL17A locus. Further, MIAT regulates the expression of protein kinase C alpha (PKCα), an upstream regulator of IL17A. A reanalysis of published single-cell RNA-seq data showed that MIAT was expressed in T cells from the synovium of RA patients. Our results demonstrate that MIAT contributes to human Th17 differentiation by upregulating several genes implicated in Th17 differentiation. High MIAT expression in T cells of RA patient synovia suggests a possible role of MIAT in Th17 mediated autoimmune pathologies.
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