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1 General aspects (0)   1.1 Epidemiology (20)   1.2 Population genetics (2)   1.3 Pathogenesis (6)   1.4 Quality of life (12)   1.5 Glaucomas as cause of blindness (5)   1.6 Prevention and screening (9) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (16)   2.2 Cornea (12)   2.3 Sclera (9)   2.4 Anterior chamber angle (10)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (10)     2.5.2 Schlemms canal (1)     2.5.3 Scleral outlet channels (0)   2.6 Aqueous humor dynamics (0)     2.6.1 Production (0)     2.6.2 Outflow (0)       2.6.2.1 Trabecular meshwork (3)       2.6.2.2 Uveoscleral (3)     2.6.3 Compostion (4)   2.7 Episcleral veins and venous pressure (0)   2.8 Iris (7)   2.9 Ciliary body (0)   2.10 Lens (0)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (4)   2.13 Retina and retinal nerve fibre layer (23)   2.14 Optic disc (23)   2.15 Optic nerve (12)   2.16 Chiasma and retrochiasmal central nervous system (12)   2.17 Stem cells (5)   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 (6)     3.4.2 Gene studies (28)   3.5 Molecular biology incl. 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Miscellaneous (28)

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Abstract #48695 Published in IGR 14-1

In vitro study of antiadipogenic profile of latanoprost, travoprost, bimatoprost, and tafluprost in human orbital preadiopocytes

Choi HY; Lee JE; Lee JW; Park HJ; Jung JH
Journal of Ocular Pharmacology and Therapeutics 2012; 28: 146-152

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PURPOSE: To investigate the effect of prostaglandin F2α (PGF2α), latanoprost, travoprost, bimatoprost, and tafluprost on human orbital preadipocyte differentiation and intracellular lipid storage, and to reveal the potential mechanisms by which topical prostaglandin analogs induce orbital fat volume reduction and cause deep superior sulcus syndrome. METHODS: Human orbital adipose precursors were treated in vitro for 24 h (day 1) with PGF2α, latanoprost, travoprost, bimatoprost, and tafluprost in their commercial formulations (1:100 dilution). Expressions of adipogenic transcription factor, peroxisome proliferator-activated receptor-gamma (PPARγ), and CCAAT-enhancer-binding protein α (C/EBPα) were determined by real-time reverse transcription-polymerase chain reaction (RT-PCR) at day 7. At 14 days, cells were stained with oil red O, intracellular lipid accumulation was evaluated by lipid absorbance, and adipocyte expression marker [Lipoprotein lipase (LPL)] was determined by real-time RT-PCR. RESULTS: Our results showed that PGF2α and topical prostaglandin analogs down-regulated the expression of PPARγ and C/EBPα, and inhibited accumulation of intra-cytoplasmic lipid droplets and expression of LPL compared with the untreated control. Comparison between the 4 drugs showed that latanoprost had the weakest antiadipogenic effect, and bimatoprost induced the most significant reduction of adipogenesis. CONCLUSION: Latanoprost, travoprost, bimatoprost, and tafluprost inhibited human preadipocyte differentiation and intracellular lipid accumulation. Morphologic and metabolic changes in orbital adipocytes caused by PGF2α analogs are a possible pathophysiologic explanation of superior eyelid deepening in patients with glaucoma.

Department of Ophthalmology, Pusan National University Hospital , Busan, Korea.

Full article

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Classification:

11.4 Prostaglandins (Part of: 11 Medical treatment)
3.6 Cellular biology (Part of: 3 Laboratory methods)
3.5 Molecular biology incl. SiRNA (Part of: 3 Laboratory methods)

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