Topical Nepafenac Inhibits Ocular Neovascularization

Takahashi, K; Saishin, Yoshitsugu; Saishin, Yumiko; Mori, Keisuke; Andõ, Akira; Yamamoto, Satoru; Oshima, Yuji; Nambu, Hiroyuki; Melia, Michele; Bingaman, David P.; Campochiaro, Peter A.

doi:10.1167/iovs.02-0346

Cited by 115 publications

(75 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…3,4 In a related manner, COX-2 has been implicated in angiogenesis, especially of tumors. 6 Although COX inhibition diminishes retinal neovascularization in ischemic models, 28 the specific involvement of COX-2 and the identity of its products in this process have not been elucidated. Our findings disclose an important role for this immediate-early gene product in proliferative retinopathy.…”

Section: Discussionmentioning

confidence: 99%

Cyclooxygenase-2 in Human and Experimental Ischemic Proliferative Retinopathy

Valamanesh²,

et al. 2003

View full text Add to dashboard Cite

Background-Intravitreal neovascular diseases, as in ischemic retinopathies, are a major cause of blindness. Because inflammatory mechanisms influence vitreal neovascularization and cyclooxygenase (COX)-2 promotes tumor angiogenesis, we investigated the role of COX-2 in ischemic proliferative retinopathy. Methods and Results-We describe here that COX-2 is induced in retinal astrocytes in human diabetic retinopathy, in the murine and rat model of ischemic proliferative retinopathy in vivo, and in hypoxic astrocytes in vitro. Specific COX-2 but not COX-1 inhibitors prevented intravitreal neovascularization, whereas prostaglandin E 2 , mainly via its prostaglandin E receptor 3 (EP 3 ), exacerbated neovascularization. COX-2 inhibition induced an upregulation of thrombospondin-1 and its CD36 receptor, consistent with the observed antiangiogenic effects of COX-2 inhibition; EP 3 stimulation reversed effects of COX-2 inhibitors on thrombospondin-1 and CD36. Conclusion-These findings point to an important role for COX-2 in ischemic proliferative retinopathy, as in diabetes.

show abstract

Section: Discussionmentioning

confidence: 99%

Cyclooxygenase-2 in Human and Experimental Ischemic Proliferative Retinopathy

Valamanesh²,

et al. 2003

View full text Add to dashboard Cite

show abstract

“…Thus, multiple cytokines, chemokines, and angiogenic factors have been identified as early participants, but their cellular source and mechanism of induction by virus infection are not clear. Studies in other models of inflammation, including ocular inflammation, have implicated cycloxygenase 2 (COX-2)-induced prostanoids as key factors in controlling the production of early inflammatory mediators (30,32,36). In addition, COX-2-induced production of prostanoids is often implicated in chronic inflammatory diseases, characterized by edema, production of chemotactic factors, and infiltration of inflammatory cells (1, 37).…”

mentioning

confidence: 99%

Role of Inflammatory Cytokine-Induced Cycloxygenase 2 in the Ocular Immunopathologic Disease Herpetic Stromal Keratitis

Biswas

Banerjee

Kim

et al. 2005

J Virol

View full text Add to dashboard Cite

Ocular infection with herpes simplex virus (HSV) results in a blinding immunoinflammatory stromal keratitis (SK) lesion. Early preclinical events include polymorphonuclear neutrophil (PMN) infiltration and neovascularization in the corneal stroma. We demonstrate here that HSV infection of the cornea results in the upregulation of the cycloxygenase 2 (COX-2) enzyme. Early after infection, COX-2 was produced from uninfected stromal fibroblasts as an indirect effect of virus infection. Subsequently, COX-2 may also be produced from other inflammatory cells that infiltrate the cornea. The induction of COX-2 is a critical event, since inhibition of COX-2 with a selective inhibitor was shown to reduce corneal angiogenesis and SK severity. The administration of a COX-2 inhibitor resulted in compromised PMN infiltration into the cornea, as well as diminished corneal vascular endothelial growth factor levels, likely accounting for the reduced angiogenic response. COX-2 stimulation by HSV infection represents a critical early event accessible for therapy and the control of SK severity.Herpetic stromal keratitis (HSK) is a chronic immunoinflammatory reaction in the corneal stroma caused by ocular infection with herpes simplex virus (HSV) (35). The pathogenesis is complex with the key lesion-producing event being the influx of inflammatory T cells that orchestrate the stromal keratitis (SK) lesions (26, 29). However, multiple events occur early after infection which, if inhibited, can control the SK lesion severity (11). These events include the production of proinflammatory mediators, prominent invasion by polymorphonuclear neutrophil (PMN) and corneal angiogenesis (11). However, the factors responsible for initiating the inflammatory and angiogenic events in the corneal stroma after virus infection are still not well understood. Thus, multiple cytokines, chemokines, and angiogenic factors have been identified as early participants, but their cellular source and mechanism of induction by virus infection are not clear. Studies in other models of inflammation, including ocular inflammation, have implicated cycloxygenase 2 (COX-2)-induced prostanoids as key factors in controlling the production of early inflammatory mediators (30,32,36). In addition, COX-2-induced production of prostanoids is often implicated in chronic inflammatory diseases, characterized by edema, production of chemotactic factors, and infiltration of inflammatory cells (1, 37). Unlike COX-1, which is a constitutive enzyme and is essential for various physiological functions, COX-2 is an inducible enzyme that is induced in a variety of cell types by diverse stimuli (41). At present, it is not known whether a COX-2-mediated inflammatory cascade represents a key event in the pathogenesis of SK.The present study was undertaken with two major objectives.First, to find out whether HSV infection causes upregulation of COX-2 expression in the cornea and, second, to investigate the role of COX-2 in SK. Our results indicate that COX-2 is expressed promptly after viru...

show abstract

“…[21] Because long-term steroid use has been associated with various complications (e.g., cataract, glaucoma, opportunistic infection), alternative treatments have been researched. Nonsteroidal anti-inflammatory drugs (NSAIDs) have also been used in the treatment of corneal neovascularization; [22,23] however, varying effectiveness and occasionally serious side effects such as corneal ulceration have limited clinical use. [24] Thermal coagulation and occlusion of vessels can also be done using laser beams.…”

Section: Discussionmentioning

confidence: 99%

Fine Needle Diathermy for Corneal Neovascularization: Initial Results

Şalkacı¹,

Çallı²,

Kandemir³

et al. 2017

South Clin Ist Euras

View full text Add to dashboard Cite

Objective: The present study is a report of first results of fine needle diathermy (FND) procedure, the method of treatment preferred in our clinic for patients with corneal neovascularization.Methods: FND was performed on 34 eyes with corneal neovascularization in 34 patients. Anterior segment color photos were taken of all patients before and after the procedure. Visual acuity and vascularization size and depth before and after procedure were compared. Number of procedures and complications were noted.Results: Causes of vascularization were lipid keratopathy with unknown primary pathology in 12 patients, herpetic keratitis in 9, bacterial keratitis in 6, corneal graft rejection in 3, fungal keratitis in 2, alkaline burn in 2, and trauma in 1 patient. All vessels were successfully occluded in 15 patients. In 7 patients, 75% of treated vessels were occluded, and 50% of treated vessels were occluded in 5 patients. FND was performed twice on 12 patients and 3 times on 4 patients. In some cases, additional procedures were successful, and in others it was determined to be insufficient. Conclusion:FND is a safe and effective treatment for corneal neovascularization in some patients; however, in some cases, the procedure is only partially effective.

show abstract

Topical Nepafenac Inhibits Ocular Neovascularization

Cited by 115 publications

References 36 publications

Cyclooxygenase-2 in Human and Experimental Ischemic Proliferative Retinopathy

Cyclooxygenase-2 in Human and Experimental Ischemic Proliferative Retinopathy

Role of Inflammatory Cytokine-Induced Cycloxygenase 2 in the Ocular Immunopathologic Disease Herpetic Stromal Keratitis

Fine Needle Diathermy for Corneal Neovascularization: Initial Results

Contact Info

Product

Resources

About