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1 General aspects (0)   1.1 Epidemiology (3)   1.2 Population genetics (0)   1.3 Pathogenesis (4)   1.4 Quality of life (8)   1.5 Glaucomas as cause of blindness (6)   1.6 Prevention and screening (7) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (4)   2.2 Cornea (14)   2.3 Sclera (10)   2.4 Anterior chamber angle (3)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (12)     2.5.2 Schlemms canal (4)     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 (0)       2.6.2.2 Uveoscleral (0)     2.6.3 Compostion (3)   2.7 Episcleral veins and venous pressure (0)   2.8 Iris (2)   2.9 Ciliary body (1)   2.10 Lens (1)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (6)   2.13 Retina and retinal nerve fibre layer (19)   2.14 Optic disc (19)   2.15 Optic nerve (0)   2.16 Chiasma and retrochiasmal central nervous system (8)   2.17 Stem cells (5)   2.20 Other (0) 3 Laboratory methods (0)   3.1 Microscopy (2)   3.2 Electron microscopy (1)   3.3 Immunohistochemistry (1)   3.4 Molecular genetics (0)     3.4.1 Linkage studies (0)     3.4.2 Gene studies (19)   3.5 Molecular biology incl. SiRNA (20)   3.6 Cellular biology (26)   3.7 Biochemistry (9)   3.8 Pharmacology (9)   3.9 Pathophysiology (10)   3.10 Immunobiology (5)   3.11 Pharmacogenetics (0)   3.12 Proteomics (2)   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 (3)     3.13.4 Other (0)   3.20 Other (0) 4 Tissue culture of ocular cells (0) 5 Experimental glaucoma; animal models (0)   5.1 Rodent (16)   5.2 Primates (2)   5.3 Other (11) 6 Clinical examination methods (0)   6.1 Intraocular pressure measurement; factors affecting IOP (0)     6.1.1 Devices, techniques (9)     6.1.2 Fluctuation, circadian rhythms (5)     6.1.3 Factors affecting IOP (8)   6.2 Tonography, aqueous flow measurement (see also 2.6) (0)   6.3 Biomicroscopy (slitlamp) (0)     6.3.1 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8 Refractive errors in relation to glaucoma (0)   8.1 Myopia (3)   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 (4)     9.1.2 Juvenile glaucoma (11)     9.1.3 Syndromes of Axenfeld, Rieger, Peters, aniridia (2)     9.1.4 Other (0)   9.2 Primary open angle glaucomas (0)     9.2.1 Ocular hypertension (4)     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 (6)   9.3 Primary angle closure glaucomas (0)     9.3.1 Acute primary angle closure glaucoma (pupillary block) (5)     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 (0)     9.3.5 Primary angle closure (2)     9.3.10 Other (0)   9.4 Glaucomas associated with other ocular and systemic disorders 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associated with intraocular tumors (3)     9.4.9 Glaucomas associated with elevated episcleral venous pressure (0)       9.4.10 Glaucomas associated with hemorrhage (1)     9.4.11 Glaucomas following intraocular surgery (0)       9.4.11.1 Ciliary block (malignant) glaucoma (1)       9.4.11.2 Glaucomas in aphakia and pseudophakia (6)       9.4.11.3 Epithelial, fibrous, and endothelial proliferation (0)       9.4.11.4 Glaucomas associated with corneal surgery (3)       9.4.11.5 Glaucomas associated with vitreoretinal surgery (1)     9.4.15 Glaucoma in relation to systemic disease (20)     9.4.20 Other (5) 10 Differential diagnosis e.g. anterior and posterior ischemic optic neuropathy (4) 11 Medical treatment (0)   11.1 General management, indication (1)   11.2 Cholinergic drugs (3)   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 (4)     11.3.5 Other (0)   11.4 Prostaglandins 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    12.8.1 Without tube implant (12)     12.8.2 With tube implant or other drainage devices (28)     12.8.3 Non-perforating (3)     12.8.4 Using laser (0)     12.8.5 Other (10)     12.8.10 Woundhealing antifibrosis (14)     12.8.11 Complications, endophthalmitis (11)   12.9 Trabeculotomy, goniotomy (4)   12.10 Cyclodestruction (3)   12.11 Cyclodialysis (1)   12.12 Cataract extraction (0)     12.12.1 Intracapsular (0)     12.12.2 Extracapsular (0)     12.12.3 Phacoemulsification (5)   12.14 Combined cataract extraction and glaucoma surgery (0)     12.14.1 Intracapsular (0)     12.14.2 Extracapsular (0)     12.14.3 Phacoemulsification (4)   12.15 Capsulotomy (0)   12.16 Vitrectomy (2)   12.17 Anesthesia (0)   12.20 Other (3) 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 (0)     13.2.3 Other (0) 14 Costing studies; pharmacoeconomics (3) 15 Miscellaneous (28)

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Abstract #71291 Published in IGR 18-3

The selective cysteinyl leukotriene receptor 1 (CysLT1R) antagonist montelukast regulates extracellular matrix remodeling

Peng J; Zhou H; Kuang G; Xie L; Tian T; Liu R
Biochemical and Biophysical Research Communications 2017; 484: 474-479

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Scar formation after filtration surgery of glaucoma is mainly caused by excessive synthesis of new extracellular matrix (ECM) and contraction of subconjunctival tissue mediated by human Tenon fibroblasts (HTFs) and the transforming growth factor (TGF-β1). Montelukast, a potent and specific cysteinyl leukotriene receptor 1 (cysLT1R) antagonist, is a licensed drug clinically used for the treatment of bronchial asthma. In this study, we investigated the effects of montelukast on the contractility of HTFs cultured in a three-dimensional collagen gel. We found that cysLT1R was expressed in HTFs. Interestingly, the expression of cysLT1R was increased in response to TGF-β1 in a dose dependent manner, suggesting its potential role in TGF-β1 induced fibrosis. Importantly, we found that montelukast inhibited TGF-β1-induced collagen gel contraction mediated by HTFs in a concentration- and time-dependent manner. In addition, TGF-β1-induced expression of MMP-1 and MMP-3, generation of fibronectin and type I collagen production, focal adhesion kinase (FAK) and paxillin phosphorylation in HTFs were also ameliorated by montelukast in a dose dependent manner. These results suggested that montelukast might provide therapeutic possibilities for inhibition of scar formation after such surgery.

Department of Ophthalmology, Wuhan General Hospital of Guangzhou Command, Southern Medical University, Wuhan, Hubei Province, 430000, China; Department of Ophthalmology, Chenzhou First People's Hospital, Chenzhou, Hunan Province, 430000, China.

Full article

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Classification:

12.8.10 Woundhealing antifibrosis (Part of: 12 Surgical treatment > 12.8 Filtering surgery)
3.8 Pharmacology (Part of: 3 Laboratory methods)
3.6 Cellular biology (Part of: 3 Laboratory methods)
11.14 Investigational drugs; pharmacological experiments (Part of: 11 Medical treatment)

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