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Glaucoma has been the leading cause of irreversible blindness worldwide. High intraocular pressure (IOP) is a high‐risk factor of glaucoma, repression of which has been the important treatment of glaucoma in clinic. Trabecular meshwork is crucial for maintaining IOP in aqueous humour out‐flow system. It is urgent to reveal the molecular mechanism of trabecular meshwork in glaucoma. Previous studies found that some pathways were related to glaucoma, such as extracellular matrix (ECM)‐receptor interaction, phosphatidylinositol 3‐kinase (PI3K)‐protein kinase B (Akt) and apoptosis. To identify novel molecules in glaucoma, we performed high‐throughput transcriptome and proteome analysis to immortal human trabecular meshwork cells (iHTM) and glaucomatous human trabecular meshwork cells (GTM3), respectively. Twenty‐six up‐regulated genes/proteins and 59 down‐regulated genes/proteins were identified as the high‐risk factors based on differential analysis, including some known factors of glaucoma. Furthermore, a glaucoma‐related protein‐protein interaction (PPI) network was constructed for investigating the function roles of risk factors. Some genes were identified as potential regulator in the pathogenesis of glaucoma based on the topology analysis and module analysis to the network. Importantly, we identified and demonstrated that CD9 played key roles in glaucoma by biological experiment. CD9 is down‐regulated in glaucoma, overexpression of CD9 can active integrin α4 (ITGA4), PI3K and Akt, which lead to the decreased apoptosis and attenuate glaucoma. All these results provide a novel molecular therapy of glaucoma.

Background: Carotid endarterectomy (CEA) is deemed to restore the blood flow of the carotid and ophthalmic arteries in patients with carotid artery stenosis. However, specific changes in visual function before and after CEA are not well understood; hence, this observational study aimed to investigate the functional and structural changes in vision after CEA in those patients. Methods: Patients with severe carotid artery stenosis (>70% with standard carotid duplex scanning or arteriography) scheduled to undergo CEA were consecutively recruited for the study between September 2015 and July 2016. All patients underwent a standardized ophthalmic examination, including intraocular pressure (IOP) measurement, slit-lamp examination, and fundus examination. Visual acuity, best corrected visual acuity (BCVA), and kinetic and static visual fields (VFs) were tested to evaluate subjective visual function. Flash and pattern visual evoked potentials (VEPs) and an electroretinogram (ERG) were measured for objective visual function. Retinal nerve fiber layer (RNFL) thickness was scanned using optical coherence tomography for structural evaluation. Results: The study involved 15 patients (11 male and 4 female, corresponding to 30 eyes; mean age 62.8 ± 5.0 years). After CEA, both uncorrected visual acuity and BCVA improved, and IOP significantly decreased from 17.41 ± 2.59 to 15.95 ± 2.50 mm Hg (P ¼ 0.0022). Kinetic VF range increased significantly (P ¼ 0.0126) as did mean sensitivity from 18.8 ± 5.5 to 20.6 ± 4.3 dB (P ¼ 0.0208), whereas mean defect decreased from 8.2 ± 5.3 to 6.5 ± 4.2 dB (P ¼ 0.025). RNFL thickness was not significantly altered. Latency of the P2 wave on flash VEP reduced significantly after CEA (P ¼ 0.0151), whereas the oscillatory potential amplitude of waveform 3 in the ERG significantly increased after CEA. Conclusions: Our results demonstrate that an improvement in carotid artery and ophthalmic artery blood flow after CEA does indeed enhance subjective and objective assessments of visual function in patients with carotid artery stenosis, including visual acuity, kinetic and static VF, P2 latency, and ocular pressure amplitude; however, it did not affect RNFL thickness.

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Background/Aims: In this study, we aimed to investigate the effects of genistein on the focal adhesion signaling pathway through its regulation of FAK. Genistein ultimately restored and alleviated estradiol-induced vascular endothelial injury. Methods: Microarray analysis was used to select differentially expressed genes. MTT assay was performed to detect the cell activity, and ROS test and NO test were performed to detect the degree of damage to HUVECs (human umbilical vein endothelial cells). The relative mRNA expression levels and protein expression levels of FAK were tested by western blot and qRT-PCR. GO functional analysis and KEGG pathway analysis were applied to predict the possible relationship between functions and related pathways, and transwell assay was used to detect cell invasion and migration. Results: FAK was highly expressed in the HUVECs treated with estradiol (HU-ESTs). Cell viability and NO level decreased, whereas ROS level increased in the HU-ESTs. Effective knockdown of FAK in HU-ESTs elevated cell viability and NO levels while suppressing ROS levels. In addition, inhibition of FAK greatly decreased cell invasion and migration, while the overexpression of FAK enhanced cell invasion and migration. KEGG further indicated focal adhesion pathways were activated. Genistein elevated HU-EST viability, and NO and ROS level increased in a concentration dependent manner. Transwell and western blot assays revealed that genistein could reduce the FAK expression levels and alleviate the damage to the HU-ESTs. Conclusion: FAK overexpression promoted invasion and migration of the HU-ESTs. However, genistein greatly suppressed FAK and estradiol-induced vascular endothelial cell injury.