Abstract：Objective: Explore the differential expression of aqueous protein in patients with primary acute angle-closure glaucoma (PAACG) with different intraocular pressure, find the possible mechanism of glaucomatous optic nerve damage, and provide experimental basis for possible targets for glaucomatous optic nerve protection. Methods: In this case-control study, a total of 88 patients (88 eyes) with primary acute angle-closure glaucoma admitted to the Ophthalmology Center of the Second Hospital of Jilin University from March 2019 to September 2020 were randomly collected. Eighty-eight selected samples were divided into two groups according to the intraocular pressure (IOP) of patients with PAACG: group A (36 samples, IOP 50 mmHg, 1 mmHg=0. 133 kPa) and group B (52 samples, IOP 21 mmHg). The above samples were divided into two cohorts: discovery cohort (group A, 26 samples; group B, 37 samples) and validation cohort (group A, 10 samples; group B, 15 samples). Their aqueous humor proteomes were analyzed by the data-independent acquisition method and by the parallel reaction monitor method (PRM), respectively. Indepenednt t-test was used to compare protein expression. Results: In this study, a total of 636 proteins were detected from 63 aqueous humor samples in groups A and B of the discovery queue, and 506 proteins were obtained for subsequent analysis after the removal of the default protein. Among them, 51 proteins were differentially expressed between the two groups (P=0.020). Moreover, 17 proteins of these 51 differential proteins were up-regulated in group A, and 34 proteins were up-regulated in group B. Besides, APOA2, TIMP1, LRP2, and VASN were randomly selected for PRM validation, and the study results demonstrated that the results in the discovery queue were consistent with those in the validation queue. Conclusions: Our study results revealed that the expression of differentially expressed proteins was associated with inflammatory response, as well as extracellular matrix remodeling in the trabecular meshwork and nerve injury. The above factors would be an essential reason for increased intraocular pressure and optic nerve injury in glaucoma.
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