ObjectiveTo investigate whether understanding of glaucoma is associated with psychological disturbance and vision-related quality of life (QoL) in patients with glaucoma.DesignA prospective, hospital-based, cross-sectional study.SettingShanghai, China.ParticipantsFive hundred patients with glaucoma were included in the study. Participants were asked to complete the glaucoma comprehension questionnaire, the Hospital Anxiety and Depression Scale (HADS) questionnaire, and the 25-item National Eye Institute Visual Functioning Questionnaire (NEI VFQ-25).Outcome measuresSociodemographic data and clinical data were collected. Multivariate adjusted linear regression analyses were performed to examine factors related to psychological disorder and QoL. The relationship between understanding of glaucoma and psychological status or QoL was analysed.ResultsThe mean age of patients was 56.5±17.2 years, and the mean duration of glaucoma was 4.6±6.3 years. About half (54.2%) of the patients had primary open angle glaucoma, 37.2% had primary angle closure glaucoma, and 8.6% had secondary glaucoma. The total score and the subscores of knowledge of glaucoma, compliance and habits were all negatively correlated with the HADS-Depression and HADS scores. For NEI VFQ-25, the total comprehension score was positively related to general vision, near activity, distance activity, social function, colour vision and the composite score. Habits had a significant influence on both HADS-Depression and the composite score of NEI VFQ-25.ConclusionsThe level of understanding about glaucoma is an independent factor negatively associated with psychological disturbance and positively associated with QoL in patients with glaucoma. However, it is a subjective factor which can be regulated, so imparting knowledge about glaucoma and establishing appropriate habits might help patients alleviate psychological disturbance and enhance their QoL.

When cells are migrating, caveolin-1, the principal protein component of caveolae, is excluded from the leading edge and polarized at the cell rear. The dynamic feature depends on a specific sequence motif that directs intracellular trafficking of the protein. Deletion mutation analysis revealed a putative polarization domain at the N terminus of caveolin-1, between amino acids 32-60. Alanine substitution identified a minimal sequence of 10 residues ( 46 TKEIDLVNRD 55 ) necessary for caveolin-1 rear polarization. Interestingly, deletion of amino acids 1-60 did not prevent the polarization of caveolin-1 in human umbilical vein endothelial cells or wild-type mouse embryonic fibroblasts because of an interaction of Cav 61-178 mutant with endogenous caveolin-1. Surprisingly, expression of the depolarization mutant in caveolin-1 null cells dramatically impeded caveolae formation. Furthermore, knockdown of caveolae formation by methyl-␤-cyclodextrin failed to prevent wild-type caveolin-1 rear polarization. Importantly, genetic depletion of caveolin-1 led to disoriented migration, which can be rescued by full-length caveolin-1 but not the depolarization mutant, indicating a role of caveolin-1 polarity in chemotaxis. Thus, we have identified a sequence motif that is essential for caveolin-1 rear polarization and caveolae formation.Caveolae are specific microdomains of the plasma membrane that were discovered more than 50 years ago (1). In endothelial cells, numerous vesicles appeared to derive from the uniformly flask-shaped invaginations, suggesting the endocytic potential of caveolae (2). Although the function of caveolae as transport vesicles mediating endocytosis and transcytosis remained obscure (3, 4), the identification, cloning, and characterization of caveolar coat proteins, caveolins, has increased our knowledge of caveolae, and a good body of evidence implicates caveolae in a specialized form of delivery of membrane components, extracellular ligands, bacterial toxins, and nonenveloped virus in several cell types (5-8). The caveolae-mediated endocytic pathway differs from that mediated by clathrincoated pits. It is sensitive to protein kinase C inhibitors and cholesterol depletion (by filipin), and in some cells it is involved in the activation of protein tyrosine kinases (9). Phosphorylation at tyrosine 14 of caveolin-1 (Cav-1) 2 may be required for the internalization of caveolae. The mechanism controlling caveolae trafficking remains unclear, but it apparently involves both microtubule and actin cytoskeletons (10). Surprisingly, using Cav-1 as a marker for caveolae, recent studies demonstrate that caveolae are rich in a variety of signaling molecules, with the implication that caveolae may function in the regulation of signal transduction. Given these views, an attractive hypothesis would be whether caveolae could carry signaling machinery to different locations of the cell to spatially organize signaling events. Indeed, Anderson and colleagues (11) have shown recently that concomitant with the relocation o...

Glaucoma is a major cause of visual impairment characterized by progressive retinal neurodegeneration. Circular RNAs are a class of endogenous noncoding RNAs that regulate gene expression in eukaryotes. In this study, we investigated the role of cZNF609 in retinal neurodegeneration induced by glaucoma.Methods: qRT-PCR and Sanger sequencing were conducted to detect cZNF609 expression pattern during retinal neurodegeneration. Immunofluorescence staining was conducted to detect the effect of cZNF609 silencing on retinal neurodegeneration in vivo. MTT assay, Ki67 staining, and PI staining were conducted to detect the effect of cZNF609 silencing on retinal glial cells and RGC function in vitro. Bioinformatics analysis, RNA pull-down assays, and in vitro studies were conducted to reveal the mechanism of cZNF609-mediated retinal neurodegeneration.Results: cZNF609 expression was significantly up-regulated during retinal neurodegeneration. cZNF609 silencing reduced retinal reactive gliosis and glial cell activation, and facilitated RGC survival in vivo. cZNF609 silencing directly regulated Müller cell function but indirectly regulated RGC function in vitro. cZNF609 acted as an endogenous miR-615 sponge to sequester and inhibit miR-615 activity, which led to increased METRN. METRN overexpression could partially rescue cZNF609 silencing-mediated inhibitory effects on retinal glial cell proliferation.Conclusion: Intervention of cZNF609 expression is a promising therapeutic strategy for retinal neurodegeneration.

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