Inhibitory Effect of Triamcinolone Acetonide on Corneal Neovascularization

Overview

Journal Graefes Arch Clin Exp Ophthalmol

Specialty Ophthalmology

Date 2005 Jul 27

PMID 16044325

Citations 14

Authors

Masatoshi Murata

Shinji Shimizu

Saburo Horiuchi

Masayuki Taira

Affiliations

Soon will be listed here.

Abstract

Background: Corneal neovascularization (NV) plays an important role in the pathogenesis of corneal disorders. Recently, triamcinolone acetonide (TA) has been reported as a potential treatment for ocular angiogenesis. However, there are no reports on the inhibitory effect of TA on the corneal NV.

Methods: Triamcinolone acetonide (2 mg) was administered to four rabbits' eyes by a subconjunctival injection immediately after a basic fibroblast growth factor (bFGF)-pellet was placed into the cornea. As a control, four eyes received an injection of distilled water. Four weeks later, the inhibition of corneal NV was evaluated as the percentage ratio of the vessel invasion area to the area that was sandwiched between the pellet and the limbus cornea. To identify the characteristic appearance of new corneal vessels, the control cornea was examined by using the antibody of vascular endothelial growth factor (VEGF). To confirm TA concentration in TA-treated corneas, the TA level was measured using high-performance liquid chromatography.

Results: Neovascularization from the limbus to the pellet was detected in control eyes 4 weeks after the bFGF pellet implantation. TA-treated eyes demonstrated the inhibition of the neovascular response to the pellet. The severity of NV as compared between control and TA-treated eyes was statistically significant (P<0.05). Morphologically, new vessel growth was shown in the control cornea, and endothelial cells of new vessels were positively stained with the antibody of VEGF. TA concentration in TA-treated corneas at 2 weeks showed 63.5+/-42.8 microg/g (n=4, mean +/- SD), while TA was not detected in control and TA-treated corneas at 4 weeks. The level of TA was effectively maintained for at least 2 weeks after the subconjunctival injection.

Conclusion: We have demonstrated that subconjunctival TA administration inhibited rabbit corneal NV. This agent may prove useful in the treatment of corneal angiogenic disorders.

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References

Blei F, Wilson E, Mignatti P, Rifkin D . Mechanism of action of angiostatic steroids: suppression of plasminogen activator activity via stimulation of plasminogen activator inhibitor synthesis. J Cell Physiol. 1993; 155(3):568-78. DOI: 10.1002/jcp.1041550315. View

Wolff J, Guerin C, Laterra J, Bressler J, Indurti R, Brem H . Dexamethasone reduces vascular density and plasminogen activator activity in 9L rat brain tumors. Brain Res. 1993; 604(1-2):79-85. DOI: 10.1016/0006-8993(93)90354-p. View

Cockerill G, Gamble J, Vadas M . Angiogenesis: models and modulators. Int Rev Cytol. 1995; 159:113-60. DOI: 10.1016/s0074-7696(08)62106-3. View

Tabata Y, Yamada K, Miyamoto S, Nagata I, Kikuchi H, Aoyama I . Bone regeneration by basic fibroblast growth factor complexed with biodegradable hydrogels. Biomaterials. 1998; 19(7-9):807-15. DOI: 10.1016/s0142-9612(98)00233-6. View

Murata M, Kador P, Sato S . Vascular endothelial growth factor (VEGF) enhances the expression of receptors and activates mitogen-activated protein (MAP) kinase of dog retinal capillary endothelial cells. J Ocul Pharmacol Ther. 2000; 16(4):383-91. DOI: 10.1089/jop.2000.16.383. View

Challa J, Gillies M, Penfold P, Gyory J, Hunyor A, Billson F . Exudative macular degeneration and intravitreal triamcinolone: 18 month follow up. Aust N Z J Ophthalmol. 1998; 26(4):277-81. DOI: 10.1111/j.1442-9071.1998.tb01330.x. View

Gimbrone Jr M, COTRAN R, Leapman S, Folkman J . Tumor growth and neovascularization: an experimental model using the rabbit cornea. J Natl Cancer Inst. 1974; 52(2):413-27. DOI: 10.1093/jnci/52.2.413. View

Loughman M, Chatzistefanou K, Gonzalez E, Flynn E, Adamis A, Shing Y . Experimental corneal neovascularisation using sucralfate and basic fibroblast growth factor. Aust N Z J Ophthalmol. 1996; 24(3):289-95. DOI: 10.1111/j.1442-9071.1996.tb01596.x. View

Ip M, Kumar K . Intravitreous triamcinolone acetonide as treatment for macular edema from central retinal vein occlusion. Arch Ophthalmol. 2002; 120(9):1217-9. View

10.

Avery R, Connor Jr T, Farazdaghi M . Systemic amiloride inhibits experimentally induced neovascularization. Arch Ophthalmol. 1990; 108(10):1474-6. DOI: 10.1001/archopht.1990.01070120122041. View

11.

Penfold P, Gyory J, Hunyor A, Billson F . Exudative macular degeneration and intravitreal triamcinolone. A pilot study. Aust N Z J Ophthalmol. 1995; 23(4):293-8. DOI: 10.1111/j.1442-9071.1995.tb00179.x. View

12.

Ishibashi T, Miki K, Sorgente N, Patterson R, Ryan S . Effects of intravitreal administration of steroids on experimental subretinal neovascularization in the subhuman primate. Arch Ophthalmol. 1985; 103(5):708-11. DOI: 10.1001/archopht.1985.01050050100026. View

13.

Killingsworth M, Sarks J, Sarks S . Macrophages related to Bruch's membrane in age-related macular degeneration. Eye (Lond). 1990; 4 ( Pt 4):613-21. DOI: 10.1038/eye.1990.86. View

14.

Oh H, Takagi H, Takagi C, Suzuma K, Otani A, Ishida K . The potential angiogenic role of macrophages in the formation of choroidal neovascular membranes. Invest Ophthalmol Vis Sci. 1999; 40(9):1891-8. View

15.

Duffin R, Weissmann B, Glasser D, Pettit T . Flurbiprofen in the treatment of corneal neovascularization induced by contact lenses. Am J Ophthalmol. 1982; 93(5):607-14. DOI: 10.1016/s0002-9394(14)77376-3. View

16.

Shweiki D, Itin A, Soffer D, Keshet E . Vascular endothelial growth factor induced by hypoxia may mediate hypoxia-initiated angiogenesis. Nature. 1992; 359(6398):843-5. DOI: 10.1038/359843a0. View

17.

Jonas J, Kreissig I, Degenring R . Intravitreal triamcinolone acetonide for pseudophakic cystoid macular edema. Am J Ophthalmol. 2003; 136(2):384-6. DOI: 10.1016/s0002-9394(03)00230-7. View

18.

Yang C, Yasukawa T, Kimura H, Miyamoto H, Honda Y, Tabata Y . Experimental corneal neovascularization by basic fibroblast growth factor incorporated into gelatin hydrogel. Ophthalmic Res. 2000; 32(1):19-24. DOI: 10.1159/000055582. View

19.

Kvanta A, Algvere P, Berglin L, Seregard S . Subfoveal fibrovascular membranes in age-related macular degeneration express vascular endothelial growth factor. Invest Ophthalmol Vis Sci. 1996; 37(9):1929-34. View

20.

Ciulla T, Criswell M, Danis R, Hill T . Intravitreal triamcinolone acetonide inhibits choroidal neovascularization in a laser-treated rat model. Arch Ophthalmol. 2001; 119(3):399-404. DOI: 10.1001/archopht.119.3.399. View