Serpiginous choroiditis (SC) is a posterior uveitis displaying a geographic pattern of choroiditis, extending from the juxtapapillary choroid and intermittently spreading centrifugally. The choroiditis involves the overlying retinal pigment epithelium, and the outer retina. This intraocular inflammation typically involves both eyes in otherwise healthy, middle-aged individuals with no familial or ethnic predilection. Pathogenesis is unclear; however, based on limited histopathologic studies, favorable response to immunosuppressive agents, and the absence of association with systemic or local infectious or noninfectious diseases, an organ-specific autoimmune inflammation seems likely to be the underlying process. Patients, particularly from tuberculosis-endemic regions, may present with fundus changes simulating SC, but show evidence of active tuberculosis and/or the presence of mycobacterial DNA in the aqueous humor. This has been referred to as serpiginous-like choroiditis, but we prefer the description multifocal serpiginoid choroiditis (MSC). We present the distinguishing features of SC and infectious multifocal serpiginoid choroiditis simulating SC. The distinction is crucial to avoid unnecessarily treating SC with antimicrobial agents. Advances in diagnostic and imaging modalities can help differentiate SC from MSC. Novel local and systemic treatment approaches improve the outcome and preserve vision in SC.
Smartphone fundus photography is a simple technique to obtain ocular fundus pictures using a smartphone camera and a conventional handheld indirect ophthalmoscopy lens. This technique is indispensable when picture documentation of optic nerve, retina, and retinal vessels is necessary but a fundus camera is not available. The main advantage of this technique is the widespread availability of smartphones that allows documentation of macula and optic nerve changes in many settings that was not previously possible. Following the well-defined steps detailed here, such as proper alignment of the phone camera, handheld lens, and the patient's pupil, is the key for obtaining a clear retina picture with no interfering light reflections and aberrations. In this paper, the optical principles of indirect ophthalmoscopy and fundus photography will be reviewed first. Then, the step-by-step method to record a good quality retinal image using a smartphone will be explained.
Citation: He S, Barron E, Ishikawa K, et al. Inhibition of DNA methylation and methyl-CpG-binding protein 2 suppresses RPE transdifferentiation: relevance to proliferative vitreoretinopathy. Invest Ophthalmol Vis Sci. 2015;56:5579-5589. DOI:10.1167/ iovs.14-16258 PURPOSE. The purpose of this study was to evaluate expression of methyl-CpG-binding protein 2 (MeCP2) in epiretinal membranes from patients with proliferative vitreoretinopathy (PVR) and to investigate effects of inhibition of MeCP2 and DNA methylation on transforming growth factor (TGF)-b-induced retinal pigment epithelial (RPE) cell transdifferentiation. METHODS.Expression of MeCP2 and its colocalization with cytokeratin and a-smooth muscle actin (a-SMA) in surgically excised PVR membranes was studied using immunohistochemistry. The effects of 5-AZA-2 0 -deoxycytidine (5-AZA-dC) on human RPE cell migration and viability were evaluated using a modified Boyden chamber assay and the colorimetric 3-(4,5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide (MTT) assay. Expression of RASAL1 mRNA and its promoter region methylation were evaluated by real-time PCR and methylationspecific PCR. Effects of 5-AZA-dC on expression of a-SMA, fibronectin (FN), and TGF-b receptor 2 (TGF-b R2) and Smad2/3 phosphorylation were analyzed by Western blotting. Effect of short interfering RNA (siRNA) knock-down of MeCP2 on expression of a-SMA and FN induced by TGFb was determined.RESULTS. MeCP2 was abundantly expressed in cells within PVR membranes where it was double labeled with cells positive for cytokeratin and a-SMA. 5-AZA-dC inhibited expression of MeCP2 and suppressed RASAL1 gene methylation while increasing expression of the RASAL1 gene. Treatment with 5-AZA-dC significantly suppressed the expression of a-SMA, FN, TGF-b R2 and phosphorylation of Smad2/3 and inhibited RPE cell migration. TGF-b induced expression of a-SMA, and FN was suppressed by knock-down of MeCP2.CONCLUSIONS. MeCP2 and DNA methylation regulate RPE transdifferentiation and may be involved in the pathogenesis of PVR.
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