Search

We characterized Müller cell gliosis induced by the activation of transient receptor potential vanilloid-type 4 (TRPV4) and assessed whether statins could modulate the gliosis. The human Müller cell line, MIO-M1, was used to analyze the gliosis caused by glaucomatous stimulation. To induce Müller gliosis in MIO-M1 cells, GSK101 was used to activate TRPV4, and Müller gliosis was evaluated by analyzing vimentin, nestin, and glial fibrillary acidic protein (GFAP) expression. The expression level of TNF-α was determined by ELISA. To evaluate the GSK101 activation of the NF-κB pathway, p65 phosphorylation was measured by Western blotting, and the nuclear translocation of p65 and IκBα phosphorylation were assessed by immunostaining. To assess the effect of statins on MIO-M1 gliosis, cells were pretreated for 24 h with statins before GSK101 treatment. Vimentin, nestin, and GFAP expression were upregulated by GSK101, while statins effectively inhibited them. The expression of TNF-α was increased by GSK101. The phosphorylation and nuclear translocation of p65 and IκBα phosphorylation, which occurs prior to p65 activation, were induced. Statins suppressed the GSK101-mediated phosphorylation of IκBα and p65 translocation. Statins can mitigate gliosis in the human Müller cell line. Because TRPV4 activation in Müller cells reflects glaucoma pathophysiology, statins may have the potential to prevent RGC death. [ABSTRACT FROM AUTHOR]

Purpose. To investigate the effect of refractive error on the physiologic thinning rate of the retinal nerve fiber layer (RNFL) in healthy eyes. Materials and Methods. This study analyzed 223 eyes of 141 healthy subjects followed for more than 5 years and underwent at least five serial spectral domain optical coherence tomography (SD-OCT) examinations. Longitudinal RNFL measurements were analyzed by linear mixed models incorporating follow-up duration, baseline RNFL thickness, spherical equivalent (SE), age, intraocular pressure, and visual field mean deviation. Thinning rates were classified according to SE into three groups: nonmyopic (NM; >0 D), mild-to-moderately myopic (MM; >–6 D and ≤0 D), and highly myopic (HM; ≤–6 D). Results. The overall slopes of change in RNFL thickness over time in the NM, MM, and HM groups were −0.305 ± 0.128, −0.294 ± 0.068, and −0.208 ± 0.097 μm/yr, respectively. Slopes of RNFL thickness changes in these groups were −0.514 ± 0.248, −0.520 ± 0.133, and −0.528 ± 0.188 μm/yr, in the superior quadrant; −0.084 ± 0.145, 0.107 ± 0.082, and −0.161 ± 0.112 μm/yr, in the temporal quadrant; −0.807 ± 0.242, −0.794 ± 0.130, and −0.727 ± 0.183 μm/yr, in the inferior quadrant; and 0.160 ± 0.157, 0.118 ± 0.084, and 0.429 ± 0.119 μm/yr, in the nasal quadrant. Overall and in all four quadrants, there was no significant difference in the rate of RNFL thickness change among the three groups. Conclusions. Refractive error did not affect the physiologic thinning rate of RNFL when assessed by SD OCT. [ABSTRACT FROM AUTHOR]

To investigate the impact of systolic and diastolic blood pressure (DBP) dip at baseline on subsequent visual field (VF) progression in eyes with normal-tension glaucoma (NTG). Prospective cohort study. This study included 119 eyes of 119 newly diagnosed NTG patients followed up for at least 2 years (average, 40.4±16.9 months). All participants underwent baseline 24-hour ambulatory blood pressure (BP) monitoring and measurements of intraocular pressure (IOP) and at least 5 serial VF examinations. Participants were followed up as outpatients at 4- to 6-month intervals. Visual field progression was defined according to Early Manifest Glaucoma Trial criteria. The associations of VF progression with systolic BP (SBP) and DBP measured during the day and at night and other clinical variables were analyzed. Factors associated with VF progression over time. During follow-up, 41 eyes (34%) showed VF progression. In the multivariate Cox regression model, lower nighttime trough DBP (hazard ratio, 0.953; P = 0.023) and greater nighttime DBP dip area (time multiplied by nighttime DBP > 10 mmHg less than mean daytime DBP; hazard ratio, 1.017; P = 0.003) at baseline were significant predictors of subsequent VF progression. None of the SBP parameters was associated with VF progression. Nocturnal DBP dip showed a greater association with VF progression than SBP dip. Nocturnal trough DBP and DBP dip area at baseline are significant predictors of subsequent VF progression in NTG. Nocturnal DBP dip may be more relevant to future VF progression than SBP dip in NTG eyes. [ABSTRACT FROM AUTHOR]