Jiang Lihong, Rong Ao, Wei Ruili, Diao Jiale, Ding Hui, Wang Wei
Department of Ophthalmology, Tongji Hospital, School of Medicine, Tongji University, Shanghai 200065, P.R. China.
Department of Ophthalmology, Zhabei Central Hospital, Jingan District, Shanghai 200070, P.R. China.
Exp Ther Med. 2020 Dec;20(6):253. doi: 10.3892/etm.2020.9383. Epub 2020 Oct 23.
The progress and achievements that have been made in tear proteomics in thyroid-associated ophthalmopathy (TAO) are critical for exploring the pathogenesis of TAO and investigating potential therapeutic targets. However, the tear proteomics of orbital decompression for disfiguring exophthalmos in inactive TAO have yet to be properly investigated. In the present study, orbital decompression was performed to repair disfiguring exophthalmos in patients with inactive TAO. Tears were collected before and after orbital decompression in patients with inactive TAO. Liquid chromatography with tandem mass spectrometry (LC-MS/MS) was performed to explore the changes in tear proteomics. Bioinformatics analyses were then employed to analyze the functions of the differentially expressed proteins (DEPs) identified by LC-MS/MS. The palpebral fissure height and exophthalmia area were significantly restored after 1 month of orbital decompression such that they approached the normal levels identified in healthy eyeballs. Among the 669 proteins identified by LC-MS/MS, 83 proteins were changed significantly between the preoperative and postoperative stages in inactive TAO patients and healthy control individuals. The DEPs were predicted to be involved in numerous signaling pathways. Bioinformatics analyses revealed that pathways associated with the immune system, metabolism, programmed cell death, vesicle-mediated transport, neuronal system and extracellular matrix organization may fulfill significant roles in orbital decompression in patients with inactive TAO. Taken together, these results provided a preliminary understanding of the mechanism of orbital decompression for disfiguring exophthalmos in inactive TAO patients.
甲状腺相关眼病（TAO）泪液蛋白质组学所取得的进展和成就对于探索TAO的发病机制以及研究潜在治疗靶点至关重要。然而，针对静止期TAO中导致眼球突出变形的眼眶减压术后泪液蛋白质组学尚未得到充分研究。在本研究中，对静止期TAO患者进行眼眶减压以修复眼球突出变形。收集静止期TAO患者眼眶减压术前和术后的泪液。采用液相色谱串联质谱（LC-MS/MS）技术来探索泪液蛋白质组学的变化。随后利用生物信息学分析来分析由LC-MS/MS鉴定出的差异表达蛋白（DEP）的功能。眼眶减压1个月后，睑裂高度和眼球突出面积显著恢复，接近健康眼球的正常水平。在通过LC-MS/MS鉴定出的669种蛋白质中，83种蛋白质在静止期TAO患者术前和术后阶段以及健康对照个体之间有显著变化。预测这些DEP参与众多信号通路。生物信息学分析表明，与免疫系统、代谢、程序性细胞死亡、囊泡介导运输、神经系统和细胞外基质组织相关的通路可能在静止期TAO患者的眼眶减压中发挥重要作用。综上所述，这些结果为理解静止期TAO患者眼眶减压修复眼球突出变形的机制提供了初步认识。
