Dataset Information

Renin Promotes STAT4 Phosphorylation to Induce IL-17 Production in Keratinocytes of Oral Lichen Planus.

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-?B 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.

SUBMITTER: Ge X

PROVIDER: S-EPMC7093809 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature

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Renin Promotes STAT4 Phosphorylation to Induce IL-17 Production in Keratinocytes of Oral Lichen Planus.

Ge Xuejun X Xie Hanting H Nguyen Tivoli T Zhao Bin B Xu Jing J Du Jie J

iScience 20200313 4

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 transcr ...[more]

PMID: 32213463

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Project description:BackgroundA growing number of studies has investigated IL-17 in OLP. However, its exact role and interactions are not fully determined. In addition, the literature investigating its salivary expression is limited. The scarcity in the literature studying lncRNAs was noticed, particularly with regards to correlating them with cytokines in OLP. In the current study, the salivary expression of lncRNA DQ786243 and IL-17 was assessed among different forms of OLP.MethodsThe study included 52 participants in four equal groups: reticular OLP, erythematous OLP, ulcerative OLP, and control group. All eligible OLP patients underwent conventional oral examination, along with basic charting of their demographic data, pain intensity using a visual analogue scale, and clinical evaluation using the Thongprasom et al. scale. The salivary expression of lncRNA DQ786243 and IL-17 was evaluated for all participants using qRT-PCR. Unstimulated whole saliva samples were used. Data were analyzed for statistical significance.ResultsNo statistically significant difference was observed when comparing the mean age and gender distribution of the studied groups. A statistically significant difference was detected when comparing pain and clinical scores in the three OLP forms. The highest expression of both salivary biomarkers was noticed in ulcerative OLP, followed by erythematous OLP and reticular OLP, then the controls, with a significant difference between the studied groups. Upon comparing the salivary expression of DQ786243 in ulcerative and erythematous OLP, no significant difference was detected. No significant difference was detected when comparing salivary expression of IL-17 in erythematous OLP to the other OLP forms.ConclusionsThe salivary expression of lncRNA DQ786243 and IL-17 was upregulated in OLP compared to healthy individuals. Besides, their expression increased when the severity of OLP was at its highest level in ulcerative OLP. There was a positive correlation between DQ786243 and IL-17. Trial registration The protocol was registered at ClinicalTrials.gov (NCT04503824). The date of registration is 07/08/2020.

Dataset Information

Renin Promotes STAT4 Phosphorylation to Induce IL-17 Production in Keratinocytes of Oral Lichen Planus.

Publications

Renin Promotes STAT4 Phosphorylation to Induce IL-17 Production in Keratinocytes of Oral Lichen Planus.

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