Department of Ophthalmology, Beijing Key Laboratory of Diagnosis and Therapy of Retinal and Choroid Diseases, Peking University People's Hospital, Beijing, China.
College of Optometry, Peking University People's Hospital, Beijing, China.
BMC Ophthalmol. 2024 Aug 19;24(1):352. doi: 10.1186/s12886-024-03584-6.
This study aimed to identify the differentially expressed proteins in the vitreous humor (VH) of eyes with and without pathologic myopia (PM), providing insights into the molecular pathogenesis.
A cross-sectional, observational study was conducted. VH samples were collected from patients undergoing vitrectomy for idiopathic epiretinal membrane (ERM), macular hole (MH), or myopic retinoschisis (MRS). Label-free quantitative proteomic analysis identified differential protein expression, with validation using ELISA.
The proteomic profiling revealed significantly higher expressions of tubulin alpha 1a (TUBA1A) and eukaryotic translation elongation factor 1 alpha 1 (EEF1A1) in PM groups (MH-PM, MRS-PM) compared to controls (MH, ERM). Conversely, xylosyltransferase 1 (XYLT1), versican core protein (VCAN), and testican-2 (SPOCK2) expressions were lower in PM. ELISA validation confirmed these findings.
Our study provides novel insights into the molecular mechanisms of PM. The differentially expressed proteins EEF1A1, TUBA1A, XYLT1, VCAN, and SPOCK2 may play crucial roles in chorioretinal cell apoptosis, scleral extracellular matrix (ECM) synthesis, and scleral remodeling in PM. These proteins represent potential new targets for therapeutic intervention in PM, highlighting the importance of further investigations to elucidate their functions and underlying mechanisms in disease pathogenesis.
本研究旨在鉴定病理性近视(PM)眼和非病理性近视(NM)眼玻璃体液(VH)中的差异表达蛋白,深入了解分子发病机制。
进行了一项横断面、观察性研究。从接受特发性黄斑前膜(ERM)、黄斑裂孔(MH)或近视性视网膜劈裂(MRS)玻璃体切除术的患者中采集 VH 样本。采用无标记定量蛋白质组学分析鉴定差异蛋白表达,并通过 ELISA 进行验证。
蛋白质组学分析显示,PM 组(MH-PM、MRS-PM)中微管蛋白α 1a(TUBA1A)和真核翻译延伸因子 1α 1(EEF1A1)的表达明显高于对照组(MH、ERM)。相反,木糖基转移酶 1(XYLT1)、核心蛋白聚糖(VCAN)和 SPOCK2 在 PM 中的表达较低。ELISA 验证证实了这些发现。
本研究为 PM 的分子机制提供了新的见解。差异表达蛋白 EEF1A1、TUBA1A、XYLT1、VCAN 和 SPOCK2 可能在脉络膜视网膜细胞凋亡、巩膜细胞外基质(ECM)合成和 PM 中的巩膜重塑中发挥关键作用。这些蛋白可能成为 PM 治疗干预的潜在新靶点,强调了进一步研究阐明其在疾病发病机制中的功能和潜在机制的重要性。