advertisement

---

1 General aspects (0)   1.1 Epidemiology (8)   1.2 Population genetics (0)   1.3 Pathogenesis (0)   1.4 Quality of life (9)   1.5 Glaucomas as cause of blindness (3)   1.6 Prevention and screening (6) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (3)   2.2 Cornea (12)   2.3 Sclera (3)   2.4 Anterior chamber angle (1)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (5)     2.5.2 Schlemms canal (1)     2.5.3 Scleral outlet channels (0)   2.6 Aqueous humor dynamics (1)     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 (0)   2.7 Episcleral veins and venous pressure (1)   2.8 Iris (1)   2.9 Ciliary body (2)   2.10 Lens (0)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (14)   2.13 Retina and retinal nerve fibre layer (17)   2.14 Optic disc (23)   2.15 Optic nerve (3)   2.16 Chiasma and retrochiasmal central nervous system (3)   2.17 Stem cells (1)   2.20 Other (0) 3 Laboratory methods (0)   3.1 Microscopy (1)   3.2 Electron microscopy (0)   3.3 Immunohistochemistry (3)   3.4 Molecular genetics (0)     3.4.1 Linkage studies (2)     3.4.2 Gene studies (17)   3.5 Molecular biology incl. SiRNA (5)   3.6 Cellular biology (20)   3.7 Biochemistry (3)   3.8 Pharmacology (12)   3.9 Pathophysiology (11)   3.10 Immunobiology (2)   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 (5)     3.13.4 Other (1)   3.20 Other (0) 4 Tissue culture of ocular cells (0) 5 Experimental glaucoma; animal models (2)   5.1 Rodent (21)   5.2 Primates (1)   5.3 Other (3) 6 Clinical examination methods (0)   6.1 Intraocular pressure measurement; factors affecting IOP (0)     6.1.1 Devices, techniques (6)     6.1.2 Fluctuation, circadian rhythms (2)     6.1.3 Factors affecting IOP (11)   6.2 Tonography, aqueous flow measurement (see also 2.6) (0)   6.3 Biomicroscopy (slitlamp) (0)     6.3.1 Anterior segment (0)     6.3.2 Posterior segment (0)   6.4 Gonioscopy (1)   6.5 Ophthalmoscopy (0)   6.6 Visual field examination and other visual function tests (0)     6.6.1 Conventional manual (0)     6.6.2 Automated (20)     6.6.3 Special methods (e.g. color, contrast, SWAP etc.) (11)   6.7 Electro-ophthalmodiagnosis (4)   6.8 Photography (0)     6.8.1 Anterior segment (3)     6.8.2 Posterior segment (4)   6.9 Computerized image analysis (0)     6.9.1 Laser scanning (0)       6.9.1.1 Confocal Scanning Laser Ophthalmoscopy (0)       6.9.1.2 Confocal Scanning Laser Polarimetry (1)     6.9.2 Optical coherence tomography (0)       6.9.2.1 Anterior (5)       6.9.2.2 Posterior (40)     6.9.5 Other (6)   6.10 Fluorescein (ICG) angiography (0)     6.10.1 Anterior segment (1)     6.10.2 Posterior segment (0)   6.11 Bloodflow measurements (12)   6.12 Ultrasonography and ultrasound biomicroscopy (8)   6.13 Provocative tests (1)   6.19 Telemedicine (1)   6.20 Progression (13)   6.30 Other (2) 8 Refractive errors in relation to glaucoma (2)   8.1 Myopia (10)   8.2 Hypermetropia (0)   8.3 Contact lenses (0)   8.4 Refractive surgical procedures (0)   8.5 Other (0) 9 Clinical forms of glaucomas (0)   9.1 Developmental glaucomas (0)     9.1.1 Congenital glaucoma, Buphthalmos (8)     9.1.2 Juvenile glaucoma (7)     9.1.3 Syndromes of Axenfeld, Rieger, Peters, aniridia (3)     9.1.4 Other (0)   9.2 Primary open angle glaucomas (0)     9.2.1 Ocular hypertension (7)     9.2.2 Other risk factors for glaucoma (3)     9.2.3 Open angle glaucoma with elevated IOP (0)     9.2.4 Normal pressure glaucoma (11)   9.3 Primary angle closure glaucomas (0)     9.3.1 Acute primary angle closure glaucoma (pupillary block) (8)     9.3.2 Chronic primary angle closure glaucoma (pupillary block) (4)     9.3.3 Plateau iris syndrome (1)     9.3.4 Primary angle closure suspect (3)     9.3.5 Primary angle closure (2)     9.3.10 Other (0)   9.4 Glaucomas associated with other ocular and systemic disorders (0)     9.4.1 Steroid-induced glaucoma (1)     9.4.2 Glaucomas associated with disorders of the cornea, conjunctiva, sclera (0)       9.4.2.1 Iridocorneal endothelial syndrome (ICE, incl. irisatrophy) (1)       9.4.2.2 Posterior polymorphous dystrophy (0)       9.4.2.3 Fuchs' endothelial dystrophy (0)       9.4.2.5 Other (0)     9.4.3 Glaucomas associated with disorders of the iris and ciliary body (0)       9.4.3.1 Pigmentary glaucoma (1)       9.4.3.5 Other (0)     9.4.4 Glaucomas associated with disorders of the lens (0)       9.4.4.1 Exfoliation syndrome (7)       9.4.4.2 Glaucomas associated with cataracts (4)       9.4.4.3 Glaucomas associated with lens dislocation (0)       9.4.4.5 Other (2)     9.4.5 Glaucomas associated with disorders of the retina, choroid and vitreous (0)       9.4.5.1 Neovascular glaucoma (3)       9.4.5.5 Other (10)     9.4.6 Glaucomas associated with inflammation, uveitis (4)     9.4.7 Glaucomas associated with ocular trauma (1)     9.4.8 Glaucomas associated with intraocular tumors (1)     9.4.9 Glaucomas associated with elevated episcleral venous pressure (1)       9.4.10 Glaucomas associated with hemorrhage (7)     9.4.11 Glaucomas following intraocular surgery (0)       9.4.11.1 Ciliary block (malignant) glaucoma (2)       9.4.11.2 Glaucomas in aphakia and pseudophakia (4)       9.4.11.3 Epithelial, fibrous, and endothelial proliferation (0)       9.4.11.4 Glaucomas associated with corneal surgery (2)       9.4.11.5 Glaucomas associated with vitreoretinal surgery (3)     9.4.15 Glaucoma in relation to systemic disease (20)     9.4.20 Other (3) 10 Differential diagnosis e.g. anterior and posterior ischemic optic neuropathy (0) 11 Medical treatment (0)   11.1 General management, indication (3)   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 (4)     11.3.4 Betablocker (3)     11.3.5 Other (0)   11.4 Prostaglandins (6)   11.5 Carbonic anhydrase inhibitors (0)     11.5.1 Systemic (1)     11.5.2 Topical (1)   11.6 Osmotic treatment (0)   11.7 Treatment of bloodflow (0)   11.8 Neuroprotection (17)   11.9 Gene therapy (1)   11.13 Combination therapy (0)     11.13.1 Betablocker and pilocarpine (0)     11.13.2 Betablocker and carbon anhydrase inhibitor (0)     11.13.3 Betablocker and brimonidine (0)     11.13.4 Betablocker and prostaglandin (1)     11.13.5 Other (1)   11.14 Investigational drugs; pharmacological experiments (8)   11.15 Other drugs in relation to glaucoma (9)   11.16 Vehicles, delivery systems, pharmacokinetics, formulation (11)   11.17 Cooperation with medical therapy e.g. persistency, compliance, adherence (0)   11.20 Other (2) 12 Surgical treatment (0)   12.1 General management, indication (1)   12.2 Laser iridotomy (4)   12.3 Laser iridoplasty (0)   12.4 Laser trabeculoplasty and other laser treatment of the angle (3)   12.7 Surgical iridectomy (0)   12.8 Filtering surgery (2)     12.8.1 Without tube implant (11)     12.8.2 With tube implant or other drainage devices (29)     12.8.3 Non-perforating (7)     12.8.4 Using laser (0)     12.8.5 Other (0)     12.8.10 Woundhealing antifibrosis (12)     12.8.11 Complications, endophthalmitis (7)   12.9 Trabeculotomy, goniotomy (2)   12.10 Cyclodestruction (1)   12.11 Cyclodialysis (0)   12.12 Cataract extraction (0)     12.12.1 Intracapsular (0)     12.12.2 Extracapsular (0)     12.12.3 Phacoemulsification (4)   12.14 Combined cataract extraction and glaucoma surgery (0)     12.14.1 Intracapsular (0)     12.14.2 Extracapsular (1)     12.14.3 Phacoemulsification (6)   12.15 Capsulotomy (0)   12.16 Vitrectomy (6)   12.17 Anesthesia (1)   12.20 Other (2) 13 Therapeutic prognosis and outcome (0)   13.1 Prognostic factors (0)   13.2 Outcome (0)     13.2.1 IOP (0)     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 (3) 15 Miscellaneous (17)

---

Abstract #75636 Published in IGR 19-2

PI3K/Akt Pathway: A Role in δ-Opioid Receptor-Mediated RGC Neuroprotection

Husain S; Ahmad A; Singh S; Peterseim C; Abdul Y; Nutaitis MJ
Investigative Ophthalmology and Visual Science 2017; 58: 6489-6499

---

PURPOSE: This study examines the role of PI3K/Akt pathway in δ-opioid receptor agonist (SNC-121)-induced RGC neuroprotection in a chronic glaucoma rat model. METHODS: Injecting hypertonic saline into the limbal veins of Brown Norway rats elevated IOP. Rats were treated either with 1 mg/kg SNC-121 or 3 mg/kg 2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride (LY-294002; PI3K/Akt inhibitor) plus SNC-121 once daily for 7 days. Pattern ERGs were recorded in response to contrast reversal of patterned visual stimuli. Retinal ganglion cells (RGC) were visualized by Fluorogold retrograde labeling. Optic nerve head (ONH) astrocytes were pretreated with PI3K/Akt inhibitors for 30 minutes followed by 1-μM SNC-121 treatment. Changes in matrix metalloproteinases (MMP-1, -2, and -3) production and PI3K/Akt activation in optic nerve and TNF-α treated ONH astrocytes were measured by immunohistochemistry and Western blotting. RESULTS: SNC-121 activates the PI3K/Akt pathway in ONH astrocytes and the retina. In ONH astrocytes, SNC-121-induced Akt activation was fully inhibited by PI3K/Akt inhibitors. A sustained decline (7-42 days post injury) in Akt activation was seen in the ocular-hypertensive retina and optic nerve. This decline is reversed to normal levels by 1-mg/kg intraperitoneally (i.p.) SNC-121 treatment. Both pattern ERG amplitudes and RGC numbers were reduced in ocular hypertensive eyes, which were significantly increased in SNC-121-treated animals. Interestingly, SNC-121-induced increase in pattern-ERG amplitudes and RGC numbers were inhibited in LY-294002 pretreated animals. Additionally, SNC-121 treatment inhibited MMP-1, -2, and -3 production from the optic nerve of ocular hypertensive rats and TNF-α-treated ONH astrocytes. CONCLUSIONS: PI3K/Akt pathway plays a crucial role in SNC-121-mediated RGC neuroprotection against glaucomatous injury.

Hewitt Laboratory of the Ola B. Williams Glaucoma Center, Department of Ophthalmology, Storm Eye Institute, Medical University of South Carolina, Charleston, South Carolina, United States.

Full article

---

Classification:

11.8 Neuroprotection (Part of: 11 Medical treatment)
3.6 Cellular biology (Part of: 3 Laboratory methods)
5.1 Rodent (Part of: 5 Experimental glaucoma; animal models)

---

• ← Previous
• Next →

---