Prostaglandin action on ciliary smooth muscle extracellular matrix metabolism: Implications for uveoscleral outflow

Lindsey, James D.; Kashiwagi, Kenji; Kashiwagi, Fumiko; Weinreb, Robert N.

doi:10.1016/s0039-6257(97)80008-2

Cited by 106 publications

(62 citation statements)

References 28 publications

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“…PGF 2α and PGF 2α -related compounds were shown to have direct effects on the expression of MMPs and tissue inhibitors of MMPs in various types of ocular tissue/ cells, such as TM, ciliary smooth muscle, iris root and sclera [70,[75][76][77][78][79]. While TM tissues appeared altered after PGF 2α treatment, until recently it was unclear if outflow facility is increased.…”

Section: Pgf 2α and Its Analoguesmentioning

confidence: 99%

Endogenous bioactive lipids and the regulation of conventional outflow facility

Wan

Woodward

Stamer

2008

Expert Review of Ophthalmology

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SummaryPerturbation of paracrine signaling within the human conventional outflow pathway influences tissue homeostasis and outflow function. For example, exogenous introduction of the bioactive lipids, sphingosine-1-phosphate, anandamide or prostaglandin F 2α , to conventional outflow tissues alters the rate of drainage of aqueous humor through the trabecular meshwork, and into Schlemm's canal. This review summarizes recent data that characterizes endogenous bioactive lipids, their receptors and associated signaling partners in the conventional outflow tract. We also discuss the potential of targeting such signaling pathways as a strategy for the development of therapeutics to treat ocular hypertension and glaucoma.

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Section: Pgf 2α and Its Analoguesmentioning

confidence: 99%

Endogenous bioactive lipids and the regulation of conventional outflow facility

Wan

Woodward

Stamer

2008

Expert Review of Ophthalmology

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“…In the present study, we decided to investigate whether clozapine-induced cyclic AMP accumulation, an important factor attributed to uveoscleral flow, is associated with ciliary muscle contractility. However, ciliary muscle contraction has been described to have a pilocarpine-like inhibitory effect on prostaglandin F 2α -induced ocular hypotension in the uveoscleral drainage pathway [Crawford and Kaufman, 1987;Yousufzai et al, 1994;Lindsey et al, 1997].…”

Section: Introductionmentioning

confidence: 99%

Ocular hypotensive, vasorelaxant and cyclic AMP intermediation activities of clozapine displaying antiglaucoma properties

et al. 1998

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“…9,11 In addition, a reduction in collagen types I, III, and IV in PGF 2␣ -treated human ciliary muscle cultures have been reported. 14 Further, a reduction in these collagens was observed in the ciliary muscle of inflamed monkey eyes previously treated with PGF 2␣ -IE, in which uveoscleral outflow was also increased. 8,34 Thus, increased degradation of ciliary muscle ECM by MMP is thought to decrease the hydraulic resistance to uveoscleral outflow, thereby lowering the IOP in the eye.…”

Section: Discussionmentioning

confidence: 84%

“…[8][9][10][11][12][13][14][15] Although studies have shown that MMPs can alter conventional outflow facility in human and animal perfused eyes, 16,17 direct evidence that MMPs participate in the FPagonist-induced modulation of IOP remains to be determined.…”

mentioning

confidence: 99%

Latanoprost-Induced Changes in Rat Intraocular Pressure: Direct or Indirect?

Husain

Yates

Crosson

2008

Journal of Ocular Pharmacology and Therapeutics

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Introduction: The topical application of prostaglandin F 2␣ (FP)-receptor agonists has been shown to significantly lower intraocular pressure (IOP) in humans and is now considered the first-line treatment for ocular hypertension. Despite the prominent role FP-receptor agonists play in the treatment of glaucoma, our understanding of how these agents lower IOP remains incomplete. The present study was designed to evaluate the role of matrix metalloproteinase (MMP) activation and the cytokine, tumor necrosis factor alpha (TNF-␣), in latanoprost-induced changes in IOP. Methods: Changes in IOP following an acute topical administration of latanoprost (60 ng) in normotensive Brown Norway rats were evaluated by means of a commercially available rebound tonometer. To examine the role of MMPs and TNF-␣ in this response, the rats were pretreated with a broad-spectrum MMP inhibitor, GM-6001 (100 g), or the TNF-␣ inhibitor, thalidomide (25 g). Results: The topical administration of latanoprost (60 ng) alone produced a biphasic change in ipsilateral IOP: an initial hypertension (4.21 Ϯ 0.52), followed by a prolonged hypotension (Ϫ4.79 Ϯ 0.65). In rats, pretreatment with GM-6001 blocked the latanoprost-induced reduction in IOP but did not prevent the initial rise in IOP. Pretreatment with thalidomide also blocked the ocular hypotension induced by latanoprost; however, thalidomide pretreatment enhanced the duration of the initial hypertension. Conclusions: These results provide evidence that the secretion and activation of MMPs and the release of TNF-␣ play a central role in the ocular hypotension induced by FP-agonists. The administration of FP-agonists appears to lower IOP directly by inducing the activation of MMPs within the ciliary body, leading to improved uveoscleral outflow and indirectly through the release of TNF-␣ within the ciliary body. Secreted TNF-␣ may then activate TNF-receptors in the uvea and trabecular meshwork, increasing both uveoscleral and conventional outflow.

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Prostaglandin action on ciliary smooth muscle extracellular matrix metabolism: Implications for uveoscleral outflow

Cited by 106 publications

References 28 publications

Endogenous bioactive lipids and the regulation of conventional outflow facility

Endogenous bioactive lipids and the regulation of conventional outflow facility

Ocular hypotensive, vasorelaxant and cyclic AMP intermediation activities of clozapine displaying antiglaucoma properties

Latanoprost-Induced Changes in Rat Intraocular Pressure: Direct or Indirect?

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