COX-2 lack of function in hypoxia-induced ocular surface inflammation

Schwartzman, Michal Laniado; Bonazzi, Albino; Mieyal, Paul A.; Mezentsev, Alexandre; Abraham, Nader G.; Dunn, Max S.

doi:10.1016/s0049-3848(03)00415-8

Cited by 8 publications

(3 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this regard, it is important to note that in a model of hypoxia-induced corneal inflammation, the induction of COX-2 expression was not associated with a parallel increase in PGE 2 formation. 53 In accordance with the induction of PGE 2 formation as a selective response to chronic injury, amplification of the PGE 2 circuit by topical treatment with PGE 2 amplified inflammatory neovascularization (Fig. 2).…”

Section: Discussionmentioning

confidence: 55%

Selective Activation of the Prostaglandin E₂Circuit in Chronic Injury-Induced Pathologic Angiogenesis

Liclican

Nguyen

Sullivan

et al. 2010

Invest. Ophthalmol. Vis. Sci.

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 55%

Selective Activation of the Prostaglandin E₂Circuit in Chronic Injury-Induced Pathologic Angiogenesis

Liclican

Nguyen

Sullivan

et al. 2010

Invest. Ophthalmol. Vis. Sci.

View full text Add to dashboard Cite

show abstract

“…Contradictory reports exist in the literature. Some groups observe that hypoxia increases COX-2 but not PGE 2 (79, 80) or prostacyclin (81) levels. Others reports indicate that hypoxia paradoxically stimulates production of prostaglandins (82), likely via induction of COX-2 expression (83).…”

Section: Lipid Metabolism and Innate Immunitymentioning

confidence: 99%

Metabolic Shifts in Immunity and Inflammation

Kominsky

Campbell

Colgan

2010

The Journal of Immunology

340

275

View full text Add to dashboard Cite

Sites of ongoing inflammation and triggered immune responses are characterized by significant changes in metabolic activity. Recent studies have indicated that such shifts in tissue metabolism result from a combination of profound recruitment of inflammatory cells (neutrophils and monocytes) and high proliferation rates among lymphocyte populations. The resultant shifts in energy supply and demand can result in metabolic acidosis and diminished delivery and/or availability of oxygen, leading to hypoxia extensive enough to trigger transcriptional and translation changes in tissue phenotype. Such phenotypic shifts can imprint fundamental changes to tissue metabolism. Here, we review recent work addressing metabolic changes and metabolic control of inflammation and immunity.

show abstract

“…In terms of COX isoforms demonstrable in corneal epithelium subsequent to experimentally induced hypoxia-derived inflammation, COX2 protein, but not COX1, was found to dramatically increase rabbit corneal epithelium after cellular hypoxia (Schwartzman et al 2003). COX2 protein has also been noted in the canine model of corneal inflammation as well (Schwartzman et al 2003; Sellars et al 2004). However, corneal inflammation as result of hypoxia was found unrelated to the presence of the inflammatory mediator PGE2 in the rabbit model.…”

Section: Classification Of Nsaidsmentioning

confidence: 99%

Topical ophthalmic NSAIDs: a discussion with focus on nepafenac ophthalmic suspension

Gaynes¹,

Onyekwuluje²

2008

OPTH

View full text Add to dashboard Cite

The removal of diclofenac sodium ophthalmic solution as a viable pharmaceutical entity in September 1999 from the US market spurred considerable interest in the general safety and effectiveness of topical ophthalmic NSAIDs for treatment of anterior segment inflammation. In late 1999 the use of topical ocular NSAIDs declined in the US as a result of incidents involving corneal melts and toxicity surrounding use of generic diclofenac. However, since the removal of diclofenac sodium ophthalmic solution from the marketplace, ophthalmic NSAIDs have regained use as viable pharmacotherapeutic entities. Moreover, several new ophthalmic NSAID products have recently been introduced for commercial use in the US including the novel chemical entity nepafenac. The purpose of this report is to revisit the use of topical ophthalmic NSAIDs for the treatment of surgically induced anterior segment inflammation with a particular focus on nepafenac. Nepafenac is unique among ophthalmic NSAIDs in that it is a prodrug deaminated to amfenac, a highly effective non-selective cyclooxygenase inhibitor. In the case of topical ophthalmic NSAIDs, practitioners should carefully weigh the cost-benefit of implementing “highly potent” new drug products because perturbations in pharmacodynamic response due to the inherent novelty in terms of chemical designs may outweigh the demonstrated replicative pharmacologic action of all topical ophthalmic NSAIDs.

show abstract

COX-2 lack of function in hypoxia-induced ocular surface inflammation

Cited by 8 publications

References 16 publications

Selective Activation of the Prostaglandin E₂Circuit in Chronic Injury-Induced Pathologic Angiogenesis

Selective Activation of the Prostaglandin E₂Circuit in Chronic Injury-Induced Pathologic Angiogenesis

Metabolic Shifts in Immunity and Inflammation

Topical ophthalmic NSAIDs: a discussion with focus on nepafenac ophthalmic suspension

Contact Info

Product

Resources

About

COX-2 lack of function in hypoxia-induced ocular surface inflammation

Cited by 8 publications

References 16 publications

Selective Activation of the Prostaglandin E2Circuit in Chronic Injury-Induced Pathologic Angiogenesis

Selective Activation of the Prostaglandin E2Circuit in Chronic Injury-Induced Pathologic Angiogenesis

Metabolic Shifts in Immunity and Inflammation

Topical ophthalmic NSAIDs: a discussion with focus on nepafenac ophthalmic suspension

Contact Info

Product

Resources

About

Selective Activation of the Prostaglandin E₂Circuit in Chronic Injury-Induced Pathologic Angiogenesis

Selective Activation of the Prostaglandin E₂Circuit in Chronic Injury-Induced Pathologic Angiogenesis