Chen Xilan, Hao Yue, Zhang Jing, Bai Yuling, Du Yongxin, Gai Qingjie, Li Xingshuang
Department of Obstetric Clinic, Shijiazhuang Maternal and Child Health Care Hospital, No. 396 Youyi South Street, Qiaoxi District, Shijiazhuang, 050000, Hebei, China.
Department of Ophthalmology, Shijiazhuang Maternal and Child Health Care Hospital, No. 396 Youyi South Street, Qiaoxi District, Shijiazhuang, 050000, Hebei, China.
Int Ophthalmol. 2025 Sep 11;45(1):377. doi: 10.1007/s10792-025-03716-x.
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.
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.
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.
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.
干眼疾病（DED）是一种多因素慢性眼表疾病，在儿科人群中的年患病率呈上升趋势。微小RNA作为生物标志物，然而miR-1298-5p在儿科干眼疾病中的作用机制仍不清楚。本研究旨在探讨miR-1298-5p在儿科干眼疾病中的作用，并为其临床治疗提供新的见解。
本研究纳入了71例儿科干眼疾病患者和68例健康对照。通过逆转录定量聚合酶链反应（RT-qPCR）对泪液中miR-1298-5p水平进行定量，同时采用酶联免疫吸附测定（ELISA）和高效液相色谱法（HPLC）检测炎症细胞因子和血清维生素A。采用Pearson相关性分析评估miR-1298-5p表达与炎症细胞因子及维生素A水平之间的关联。多因素逻辑回归分析确定儿科干眼疾病的独立危险因素。在人角膜上皮细胞中建立体外脂多糖（LPS）刺激的儿科干眼疾病模型，然后抑制miR-1298-5p以评估细胞凋亡和炎症反应。
炎症因子、维生素A水平和户外活动时间是儿科干眼疾病的重要危险因素。儿科干眼疾病患儿泪液中miR-1298-5p水平比健康对照组高1.5倍（P＜0.001）。它与白细胞介素-6（IL-6，r = 0.687）、肿瘤坏死因子-α（TNF-α，r = 0.604）和白细胞介素-1β（IL-1β，r = 0.610）呈强正相关，与维生素A呈负相关（r = -0.566）。多因素分析显示，miR-1298-5p是儿科干眼疾病最强的预测因子（比值比[OR]=17.08，95%置信区间[CI]为6.13-47.55）。在体外，抑制miR-1298-5p可减少LPS诱导的人角膜上皮细胞凋亡，并抑制IL-6、TNF-α和IL-1β炎症因子的分泌。
miR-1298-5p是一种新的儿科干眼疾病生物标志物，与炎症和维生素A相关。它通过凋亡/炎症途径加重角膜损伤，为治疗提供了靶点和作用机制方面的见解。
