ArticleiScience2020
Renin Promotes STAT4 Phosphorylation to Induce IL-17 Production in Keratinocytes of Oral Lichen Planus.
Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- A Systematic Review of Interleukin-17 in Oral Lichen Planus: From Etiopathogenesis to Treatment.Clinical medicine & research · 2023Pooled it
- Aberrant Accumulation of Cell-Free DNA Activates the cGAS-STING-TBK1 Pathway of γδ T Cells to Promote the Inflammatory Responses in Oral Lichen Planus.Inflammation · 2026Article
- Elucidating the role of lipid metabolism dysregulation in the transition from oral lichen planus to oral squamous cell carcinoma.Journal of translational medicine · 2025Article
- Distinct Variations in Gene Expression and Cell Composition across Lichen Planus Subtypes.International journal of molecular sciences · 2024Article
- METTL14-upregulated miR-6858 triggers cell apoptosis in keratinocytes of oral lichen planus through decreasing GSDMC.Communications biology · 2023Article
- Comprehensive Insight into Lichen Planus Immunopathogenesis.International journal of molecular sciences · 2023Review
- The mechanism on Prevotella melaninogenica promoting the inflammatory progression of oral lichen planus.Clinical and experimental immunology · 2022Article
- 1,25(OH)Journal of cellular and molecular medicine · 2022Article
- Probiotics as Potential Biological Immunomodulators in the Management of Oral Lichen Planus: What's New?International journal of molecular sciences · 2022Review
- Identification of Potential Key Biomarkers and Immune Infiltration in Oral Lichen Planus.Disease markers · 2022Article
- Oral lichen planus: a microbiologist point of view.International microbiology : the official journal of the Spanish Society for Microbiology · 2021Review
- Clinical Values of miR-23a-3p in Oral Lichen Planus and Its Role in Keratinocyte Proliferation and Inflammatory Response.Journal of inflammation research · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-17 (IL-17) is highly expressed in the epithelial layer of oral lichen planus (OLP), but the underlying mechanism for IL-17 overexpression remains unknown. Here, we identify renin that is induced by NF-κB pathway contributes to the increase of IL-17 in human oral keratinocytes (HOKs). We describe that the release of cellular renin leads to the phosphorylation of Janus kinase 2 (JAK2) protein. The phosphorylated JAK2 recruits and activates the signal transducer and activator of transcription 4 (STAT4) by phosphorylating STAT4's tyrosine residue 693 (Tyr693). The now-activated STAT4 translocates into nucleus and binds to the promoter region of IL-17 gene in HOKs. Genetic interference of renin restores IL-17 levels in OLP cell models. Collectively, our results reveal that renin upregulates IL-17 expression by enhancing STAT4 phosphorylation. This discovery unveils an underpinning by which IL-17 is increased in oral keratinocytes and provides potential targeted therapies for OLP patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.