Effect of Latanoprost on the Extracellular Matrix of the Ciliary Muscle. A Study on Cultured Cells and Tissue Sections

Ocklind, Anette

doi:10.1006/exer.1998.0508

Cited by 166 publications

(92 citation statements)

References 31 publications

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“…Extensive studies have demonstrated prostaglandin-related decreases in TM cell contractility and outflow resistance of organ-cultured anterior segments [121][122][123]. The overall mechanisms through which prostaglandins enhance AH outflow remain to be fully elucidated; however, it is widely accepted that remodeling of the ECM plays a part [124][125][126][127], and it is of note that upregulation in MMP expression, through activation of prostaglandin receptors, may be involved [89,128]. However, the unique receptor profile for each analog may induce ECM modulation via different cascade pathways.…”

Section: Traditional Topical Medications In the Management Of Glaucomamentioning

confidence: 99%

Open-angle glaucoma: therapeutically targeting the extracellular matrix of the conventional outflow pathway

O’Callaghan

Cassidy

Humphries

2017

Expert Opinion on Therapeutic Targets

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Introduction:Ocular hypertension in open-angle glaucoma is caused by a reduced rate of removal of aqueous humour (AH) from the eye, with the majority of AH draining from the anterior chamber through the conventional outflow pathway, comprising the trabecular meshwork (TM) and Schlemm's Canal. Resistance to outflow is generated, in part, by the extracellular matrix (ECM) of the outflow tissues. Current pressure-lowering topical medications largely suppress AH production, or enhance its clearance through the unconventional pathway. However, therapies targeting the ECM of the conventional pathway in order to decrease intraocular pressure have become a recent focus of attention. Areas covered: We discuss the role of ECM of the TM in outflow homeostasis and its relevance as a target for glaucoma therapy, including progress in development of topical eye formulations, together with gene therapy approaches based on inducible, virally-mediated expression of matrix metalloproteinases to enhance aqueous outflow. Expert opinion: There remains a need for improved glaucoma medications that more specifically act upon sites causative to glaucoma pathogenesis. Emerging strategies targeting the ECM of the conventional outflow pathway, or associated components of the cytoskeleton of TM cells, involving new pharmacological formulations or genetically-based therapies, are promising avenues of future glaucoma treatment. ARTICLE HISTORY

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Section: Traditional Topical Medications In the Management Of Glaucomamentioning

confidence: 99%

Open-angle glaucoma: therapeutically targeting the extracellular matrix of the conventional outflow pathway

O’Callaghan

Cassidy

Humphries

2017

Expert Opinion on Therapeutic Targets

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“…The main collagens include collagen type I and type III [118][119][120], type IV [118][119][120][121], type VI [120][121][122], and collagen type XIII [123]. While most collagens showed an even distribution within the ciliary muscle, collagen type VI was only sparse within the muscle bundles and more dominant in the outer portion towards the sclera.…”

Section: Extracellular Componentsmentioning

confidence: 99%

“…While most collagens showed an even distribution within the ciliary muscle, collagen type VI was only sparse within the muscle bundles and more dominant in the outer portion towards the sclera. Additional demonstrated extracellular matrix proteins in the human ciliary muscle include fibronectin and laminin [118,120,121]; own unpublished observations showed a dense network of fibrillin and fibronectin, but only single fine vitronectin fibrils around human ciliary muscle cells.…”

Section: Extracellular Componentsmentioning

confidence: 99%

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Morphologic characteristics of the human ciliary muscle

May¹

2017

New Front Ophthalmol

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The present review focusses on the morphological characteristics of the normal human ciliary muscle. It develops in the second and third trimenon during pregnancy but continues to change after birth with developing accommodation. The mature muscle forms three distinguishable portions which are connected but show individual characteristics. The outer portion origins and inserts with tendon-like structures, while the inner portion forms a sphincter-like appearance. The distinct different innervation is not yet completely described, nor exist portion-dependent summaries of the cytological characteristics. The specific intracellular, membraneous, and extracellular components described in the literature are listed and supplemented with own observations.

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“…[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.…”

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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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Effect of Latanoprost on the Extracellular Matrix of the Ciliary Muscle. A Study on Cultured Cells and Tissue Sections

Cited by 166 publications

References 31 publications

Open-angle glaucoma: therapeutically targeting the extracellular matrix of the conventional outflow pathway

Open-angle glaucoma: therapeutically targeting the extracellular matrix of the conventional outflow pathway

Morphologic characteristics of the human ciliary muscle

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

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