基质
免疫印迹
生物
角膜
发病机制
污渍
隐形眼镜
间质细胞
细胞生物学
免疫学
免疫组织化学
医学
癌症研究
眼科
生物化学
基因
神经科学
作者
Manli Deng,Min Li,Lin Liu,Yuehui Shi,Lina Sun,Xiaoyun Ma,Jun Zou
标识
DOI:10.1016/j.clae.2023.101820
摘要
To investigate the association between proteomic changes and potential pathogenesis in the human cornea with respect to the duration of wearing soft contact lenses (SCLs).A total of 96 corneal stroma samples, obtained via small incision lenticule extraction (SMILE), were equally grouped according to the duration of wearing SCL: 0Y, did not wear SCL; 5Y, wore SCL for<5 years; 5-10Y, wore SCL for 5-10 years; O10Y, wore SCL for>10 years. Liquid chromatography-tandem mass spectrometry was used to identify and quantify protein profiles in the corneal stroma. Expression levels of CO1A1, CO4A1, NFKB1, and IL6RB were determined using western blot and immunohistochemistry analysis.This study quantified a total of 5,668 proteins across samples and identified 2,379 differentially expressed proteins (DEPs) with significantly increased abundance in the three SCL-wearing groups compared with that in the non-SCL-wearing group. Compared with those in the 0Y group, the molecular functions of DEPs in the 5Y, 5-10Y, and O10Y groups were mainly related to translation regulator activity, antigen binding, peptidase inhibitor activity, participation in extracellular matrix (ECM) production, complement activation, and inflammatory responses. Pathway enrichment analysis of DEPs showed that the sphingolipid, phosphatidylinositol 3-kinase-protein kinase B, and hypoxia-inducible factor-1 signaling pathways were activated in the human corneal stroma after long-term SCL use.Inflammation-related proteomic components in human corneal stroma increased after long-term use of SCL and may act as an essential factor in the molecular pathogenesis of corneal stroma damage.
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