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Published on: June 7, 2017
Upregulated miR-1298-5p sparks inflammatory onset and orchestrates pediatric dry eye disease progression
Xilan Chen1, Yue Hao2, Jing Zhang3
1Department of Obstetric Clinic, Shijiazhuang Maternal and Child Health Care Hospital, No. 396 Youyi South Street, Qiaoxi District, Shijiazhuang, 050000, Hebei, China.
Purpose:
Dry eye disease (DED) is a multifactorial chronic ocular surface disorder with increasing annual prevalence in the pediatric population. MicroRNAs serve as biomarkers, yet the mechanistic role of miR-1298-5p in pediatric DED remains unclear. This study aims to investigate the role of miR-1298-5p in PDED and provide new insights into its clinical treatment.
Methods:
The study enrolled 71 PDED and 68 healthy controls. Tear miR-1298-5p levels were quantified via RT-qPCR, while ELISA and HPLC measured inflammatory cytokines and serum vitamin A. Pearson correlation analysis evaluated associations between miR-1298-5p expression and inflammatory cytokines and vitamin A levels. Multivariate logistic regression identified independent risk factors for PDED. An in vitro LPS-stimulated PDED model was established in human corneal epithelial cells, followed by miR-1298-5p inhibition to assess apoptosis and inflammation.
Results:
Inflammatory factors, vitamin A levels, and outdoor activity time were significant risk factors for pediatric PDED. The level of miR-1298-5p in the tears of children with PDED is 1.5 times higher than that in the healthy control group (P < 0.001). It shows a strong positive correlation with IL-6 (r = 0.687), TNF-α (r = 0.604), and IL-1β (r = 0.610), and a negative correlation with vitamin A (r = -0.566). Multivariate analysis showed that miR-1298-5p was the strongest predictor of PDED (OR = 17.08, 95% CI 6.13-47.55). In vitro, miR-1298-5p inhibition reduced LPS-induced HCEC apoptosis and inhibited the secretion of IL-6, TNF-α, and IL-1β inflammatory factors.
Conclusion:
miR-1298-5p emerges as a novel PDED biomarker, correlating with inflammation and vitamin A. It exacerbates corneal damage through apoptotic/inflammatory pathways, offering therapeutic targets and mechanistic insights.
Insights
Pediatric dry eye disease (PDED) involves elevated miR-1298-5p levels, correlating with inflammation and vitamin A deficiency. Inhibiting miR-1298-5p reduces corneal cell apoptosis and inflammation, suggesting its therapeutic potential.
Area of Science:
- Ophthalmology
- Molecular Biology
- Biomarker Discovery
Background:
- Pediatric dry eye disease (PDED) is a growing concern with unclear underlying mechanisms.
- MicroRNAs are potential biomarkers, but the role of miR-1298-5p in PDED is not well understood.
Purpose of the Study:
- To investigate the role of miR-1298-5p in pediatric dry eye disease (PDED).
- To explore miR-1298-5p as a potential biomarker and therapeutic target for PDED.
Main Methods:
- Quantified tear miR-1298-5p, inflammatory cytokines (IL-6, TNF-α, IL-1β), and serum vitamin A in PDED patients and controls.
- Utilized RT-qPCR, ELISA, and HPLC for measurements.
- Established an in vitro LPS-stimulated human corneal epithelial cell model to assess the effects of miR-1298-5p inhibition on apoptosis and inflammation.
Main Results:
- Children with PDED showed significantly higher tear miR-1298-5p levels compared to healthy controls.
- miR-1298-5p positively correlated with IL-6, TNF-α, and IL-1β, and negatively with vitamin A.
- miR-1298-5p was identified as the strongest independent predictor of PDED.
- In vitro, inhibiting miR-1298-5p reduced LPS-induced apoptosis and inflammatory cytokine secretion in corneal cells.
Conclusions:
- miR-1298-5p is a novel and significant biomarker for pediatric dry eye disease.
- It is closely associated with ocular inflammation and vitamin A levels in PDED.
- miR-1298-5p contributes to corneal damage via apoptotic and inflammatory pathways, presenting a potential therapeutic target.
