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1 General aspects (0)   1.1 Epidemiology (7)   1.2 Population genetics (1)   1.3 Pathogenesis (3)   1.4 Quality of life (14)   1.5 Glaucomas as cause of blindness (6)   1.6 Prevention and screening (7) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (14)   2.2 Cornea (20)   2.3 Sclera (10)   2.4 Anterior chamber angle (3)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (11)     2.5.2 Schlemms canal (3)     2.5.3 Scleral outlet channels (1)   2.6 Aqueous humor dynamics (0)     2.6.1 Production (0)     2.6.2 Outflow (0)       2.6.2.1 Trabecular meshwork (4)       2.6.2.2 Uveoscleral (0)     2.6.3 Compostion (3)   2.7 Episcleral veins and venous pressure (0)   2.8 Iris (5)   2.9 Ciliary body (0)   2.10 Lens (1)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (24)   2.13 Retina and retinal nerve fibre layer (33)   2.14 Optic disc (27)   2.15 Optic nerve (5)   2.16 Chiasma and retrochiasmal central nervous system (6)   2.17 Stem cells (7)   2.20 Other (0) 3 Laboratory methods (0)   3.1 Microscopy (1)   3.2 Electron microscopy (0)   3.3 Immunohistochemistry (1)   3.4 Molecular genetics (0)     3.4.1 Linkage studies (1)     3.4.2 Gene studies (16)   3.5 Molecular biology incl. 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associated with intraocular tumors (6)     9.4.9 Glaucomas associated with elevated episcleral venous pressure (0)       9.4.10 Glaucomas associated with hemorrhage (5)     9.4.11 Glaucomas following intraocular surgery (2)       9.4.11.1 Ciliary block (malignant) glaucoma (3)       9.4.11.2 Glaucomas in aphakia and pseudophakia (8)       9.4.11.3 Epithelial, fibrous, and endothelial proliferation (0)       9.4.11.4 Glaucomas associated with corneal surgery (8)       9.4.11.5 Glaucomas associated with vitreoretinal surgery (8)     9.4.15 Glaucoma in relation to systemic disease (47)     9.4.20 Other (1) 10 Differential diagnosis e.g. anterior and posterior ischemic optic neuropathy (4) 11 Medical treatment (0)   11.1 General management, indication (4)   11.2 Cholinergic drugs (0)   11.3 Adrenergic drugs (0)     11.3.1 Epinephrine (0)     11.3.2 Thymoxamine, dapiprazole (0)     11.3.3 Apraclonidine, brimonidine (3)     11.3.4 Betablocker (8)     11.3.5 Other (0)   11.4 Prostaglandins 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    12.8.1 Without tube implant (20)     12.8.2 With tube implant or other drainage devices (59)     12.8.3 Non-perforating (15)     12.8.4 Using laser (0)     12.8.5 Other (2)     12.8.10 Woundhealing antifibrosis (16)     12.8.11 Complications, endophthalmitis (22)   12.9 Trabeculotomy, goniotomy (13)   12.10 Cyclodestruction (13)   12.11 Cyclodialysis (0)   12.12 Cataract extraction (0)     12.12.1 Intracapsular (0)     12.12.2 Extracapsular (0)     12.12.3 Phacoemulsification (12)   12.14 Combined cataract extraction and glaucoma surgery (0)     12.14.1 Intracapsular (0)     12.14.2 Extracapsular (0)     12.14.3 Phacoemulsification (6)   12.15 Capsulotomy (0)   12.16 Vitrectomy (0)   12.17 Anesthesia (0)   12.20 Other (6) 13 Therapeutic prognosis and outcome (0)   13.1 Prognostic factors (0)   13.2 Outcome (0)     13.2.1 IOP (1)     13.2.2 Visual field (0)       13.2.2.1 Progression (0)       13.2.2.2 Improvement (1)     13.2.3 Other (0) 14 Costing studies; pharmacoeconomics (6) 15 Miscellaneous (41)

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Abstract #77068 Published in IGR 19-3

Targeting circular RNA-ZRANB1 for therapeutic intervention in retinal neurodegeneration

Wang JJ; Shan K; Shan K; Liu BH; Liu BH; Liu C; Zhou RM; Zhou RM; Li XM; Li XM; Dong R; Dong R; Zhang SJ; Zhang SH; Wu JH; Yan B; Yan B
Cell Death and Disease 2018; 9: 540

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Glaucoma is a neurodegenerative disease characterized by retinal ganglion cell (RGC) loss, optic disc excavation, and progressive visual field loss. Direct or indirect ameliorating retinal neurodegeneration is a promising therapeutic therapy for glaucoma. Circular RNAs (circRNAs) are a class of covalently closed circular RNA transcripts and have emerged as potential regulators in several neurodegenerative diseases. In this study, we show that cZRANB1 expression is significantly upregulated in retinal neurodegeneration induced by glaucoma. cZRANB1 knockdown decreases retinal reactive gliosis, glial cell activation, and facilitates RGC survival in vivo. cZRANB1 knockdown directly regulates Müller cell function and indirectly regulates RGC function in vitro. cZRANB1 acts as miRNA sponge to regulate Müller cell function through cZRANB1/miR-217/RUNX2 network. Intervention of cZRANB1 expression would become an effective strategy for treating retinal neurodegeneration.

Full article

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Classification:

3.5 Molecular biology incl. SiRNA (Part of: 3 Laboratory methods)
11.8 Neuroprotection (Part of: 11 Medical treatment)

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