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1 General aspects (0)   1.1 Epidemiology (9)   1.2 Population genetics (1)   1.3 Pathogenesis (0)   1.4 Quality of life (11)   1.5 Glaucomas as cause of blindness (11)   1.6 Prevention and screening (13) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (2)   2.2 Cornea (14)   2.3 Sclera (8)   2.4 Anterior chamber angle (3)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (6)     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 (1)       2.6.2.1 Trabecular meshwork (3)       2.6.2.2 Uveoscleral (0)     2.6.3 Compostion (1)   2.7 Episcleral veins and venous pressure (0)   2.8 Iris (6)   2.9 Ciliary body (0)   2.10 Lens (0)   2.11 Vitreous body (1)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (2)   2.13 Retina and retinal nerve fibre layer (21)   2.14 Optic disc (20)   2.15 Optic nerve (4)   2.16 Chiasma and retrochiasmal central nervous system (4)   2.17 Stem cells (3)   2.20 Other (0) 3 Laboratory methods (0)   3.1 Microscopy (0)   3.2 Electron microscopy (1)   3.3 Immunohistochemistry (0)   3.4 Molecular genetics (0)     3.4.1 Linkage studies (1)     3.4.2 Gene studies (14)   3.5 Molecular biology incl. SiRNA (10)   3.6 Cellular biology (23)   3.7 Biochemistry (6)   3.8 Pharmacology (12)   3.9 Pathophysiology (9)   3.10 Immunobiology (6)   3.11 Pharmacogenetics (0)   3.12 Proteomics (0)   3.13 In vivo imaging (0)     3.13.1 Laser Scanning (0)       3.13.1.1 Confocal Scanning Laser Ophthalmoscopy (0)       3.13.1.2 Confocal Scanning Laser Polarimetry (0)     3.13.2 Optical Coherence Tomography (0)       3.13.2.1 Anterior Segment (0)       3.13.2.2 Posterior Segment (0)     3.13.3 RGC Imaging (1)     3.13.4 Other (0)   3.20 Other (1) 4 Tissue culture of ocular cells (0) 5 Experimental glaucoma; animal models (0)   5.1 Rodent (12)   5.2 Primates (2)   5.3 Other (8) 6 Clinical examination methods (0)   6.1 Intraocular pressure measurement; factors affecting IOP (1)     6.1.1 Devices, techniques (13)     6.1.2 Fluctuation, circadian rhythms (8)     6.1.3 Factors affecting IOP (15)   6.2 Tonography, aqueous flow measurement (see also 2.6) (1)   6.3 Biomicroscopy (slitlamp) (0)     6.3.1 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    12.8.1 Without tube implant (22)     12.8.2 With tube implant or other drainage devices (25)     12.8.3 Non-perforating (4)     12.8.4 Using laser (0)     12.8.5 Other (1)     12.8.10 Woundhealing antifibrosis (15)     12.8.11 Complications, endophthalmitis (7)   12.9 Trabeculotomy, goniotomy (10)   12.10 Cyclodestruction (5)   12.11 Cyclodialysis (0)   12.12 Cataract extraction (0)     12.12.1 Intracapsular (0)     12.12.2 Extracapsular (0)     12.12.3 Phacoemulsification (7)   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 (5)   12.17 Anesthesia (2)   12.20 Other (2) 13 Therapeutic prognosis and outcome (0)   13.1 Prognostic factors (1)   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 (0)     13.2.3 Other (0) 14 Costing studies; pharmacoeconomics (5) 15 Miscellaneous (27)

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Abstract #65914 Published in IGR 17-3

Ribonuclease 5 coordinates signals for the regulation of intraocular pressure and inhibits neural apoptosis as a novel multi-functional anti-glaucomatous strategy

Kim KW; Park SH; Oh DH; Lee SH; Lim KS; Joo K; Chun YS; Chang SI; Min KM; Kim JC
Biochimica et Biophysica Acta 2016; 1862: 145-154

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Glaucoma is a vision-threatening disorder characterized by progressive death of retinal ganglion cells (RGCs), although little is known about therapeutic milestones. Due to its complex and multifactorial pathogenesis, multipronged therapeutic approach is needed. Angiogenin (ANG), now called ribonuclease (RNase) 5, has been previously known as angiogenic factor and more recently its biologic activity is extended to promoting cell survival via its ribonucleolytic activity. Here, we revealed the defect of ANG in human glaucomatous trabecular meshwork (TM) cells and identified novel multiple functions of ANG as an anti-glaucomatous strategy. ANG was highly expressed in normal eyes and normal TM cells compared to glaucomatous TM cells. ANG induced intraocular pressure (IOP) lowering in rat models of both normal and elevated IOP, and as a possible mechanism, activated Akt-mediated signals for nitric oxide (NO) production, an important regulator of IOP in glaucomatous TM cell. Moreover, we demonstrated ANG-induced production of matrix metalloproteinase (MMP)-1 and -3 and rho-kinase inhibition for TM remodeling. For anti-glaucomatous defense optimization, ANG not only elicited immune-modulative pathways via indolamine 2,3-dioxygenase (IDO) activation in TM cells and suppression of Jurkat T cells, but also rescued neural stem cells (NSCs) from apoptosis induced by glaucomatous stress. These results demonstrate that novel multi-functional effects of ANG may have benefits against glaucoma in ocular tissues.

Department of Ophthalmology, College of Medicine, Chung-Ang University Hospital, Seoul, Republic of Korea; Graduate School of Chung-Ang University, College of Medicine, Seoul, Republic of Korea.

Full article

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Classification:

3.6 Cellular biology (Part of: 3 Laboratory methods)
3.5 Molecular biology incl. SiRNA (Part of: 3 Laboratory methods)
3.9 Pathophysiology (Part of: 3 Laboratory methods)

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