Effects of Prostaglandin F2αand Carbachol on MAP Kinases, Cytosolic Phospholipase A2and Arachidonic Acid Release in Cat Iris Sphincter Smooth Muscle Cells

Husain, Shahid; Abdel‐Latif, Ata A.

doi:10.1006/exer.2001.0991

Cited by 12 publications

(7 citation statements)

References 31 publications

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“…20 Prostaglandin F 2␣ activates both ERK1/2 and p38 signaling pathways in smooth muscle cells of the iris sphincter. 21 In the present study, latanoprost induced activation of the MAPKs ERK1/2, p38, and JNK in HTFs in a time-and concentration-dependent manner. Consistent with these findings, latanoprost-induced Effect of a PLC inhibitor on latanoprost-induced collagen gel contraction mediated by HTFs.…”

Section: Discussionsupporting

confidence: 51%

Induction by Latanoprost of Collagen Gel Contraction Mediated by Human Tenon Fibroblasts: Role of Intracellular Signaling Molecules

Liu¹,

Ko²,

Yanai³

et al. 2008

Invest. Ophthalmol. Vis. Sci.

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Section: Discussionsupporting

confidence: 51%

Induction by Latanoprost of Collagen Gel Contraction Mediated by Human Tenon Fibroblasts: Role of Intracellular Signaling Molecules

Liu¹,

Ko²,

Yanai³

et al. 2008

Invest. Ophthalmol. Vis. Sci.

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“…For example, PKC, MAP kinase and the small G protein, Rho were suggested to be involved in the PGF 2α induced expression of Cyr61 and CTGF. P38 and P42/44 MAP kinase pathways were stimulated by PGF 2α analogues in cat iris, human ciliary muscle cells , and non-pigmented epithelial cells that may result in an increase in the secretion and activation of MMPs [81][82][83]. In addition, it was suggested that the prior up-regulation of COX-2 was involved in latanoprost-stimulated expression of MMP-1 [81].…”

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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“…This is an important finding as little is known about the molecular events that connect latanoprost treatment with IOP reduction. Latanoprost has been shown to phosphorylate myosin light chain kinase in the iris, 19–21 indicating a role for latanoprost in cell relaxation. However, STC-1 is the first individual molecule that has been identified as a key downstream effector of latanoprost signaling.…”

Section: Discussionmentioning

confidence: 99%

“…7,19–21 While latanoprost binds to FP and FP-like receptors in cells of the conventional outflow pathway, 22 what happens following receptor activation and the identity of critical effector molecules necessary for increasing outflow facility are unknown. Identifying latanoprost-induced effector molecules will allow for a better understanding of the pathophysiology behind the treatment of ocular hypertension.…”

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confidence: 99%

Stanniocalcin-1 Is an Ocular Hypotensive Agent and a Downstream Effector Molecule That Is Necessary for the Intraocular Pressure–Lowering Effects of Latanoprost

Roddy

Viker

Winkler

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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PurposeTo identify downstream signaling molecules through which intraocular pressure (IOP) is lowered following treatment with the prostaglandin analog latanoprost.MethodsTotal RNA and protein isolated from primary human Schlemm's canal cells (n = 3) treated with latanoprost (free acid; 100 nM) were processed for quantitative PCR and Western blot analysis. IOP was evaluated in stanniocalcin-1 (STC-1−/−) and wild-type mice following treatment with latanoprost or Rho kinase inhibitor Y27632. Human anterior segment pairs (n = 8) were treated with recombinant STC-1 (5, 50, or 500 ng/mL) and pressure was recorded using custom-designed software. The effect of recombinant STC-1 (0.5 mg/mL) on IOP was evaluated in wild-type mice. Tissue morphology was evaluated by light and transmission electron microscopy.ResultsIncreased STC-1 mRNA (4.0- to 25.2-fold) and protein expression (1.9- to 5.1-fold) was observed within 12 hours following latanoprost treatment. Latanoprost reduced IOP in wild-type mice (22.0% ± 1.9%), but had no effect on STC-1−/− mice (0.5% ± 0.7%). In contrast, Y27632 reduced IOP in both wild-type (12.5% ± 1.2%) and in STC-1−/− mice (13.1% ± 2.8%). Human anterior segments treated with STC-1 (500 ng/mL) showed an increase in outflow facility (0.15 ± 0.03 to 0.27 ± 0.09 μL/min/mm Hg) while no change was observed in paired vehicle-treated controls. Recombinant STC-1 reduced IOP in wild-type mice by 15.2% ± 3.0%. No observable morphologic changes were identified between treatment groups when evaluated by microscopy.ConclusionsLatanoprost-induced reduction of IOP is mediated through the downstream signaling molecule STC-1. When used by itself, STC-1 exhibits ocular hypotensive properties.

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Effects of Prostaglandin F2αand Carbachol on MAP Kinases, Cytosolic Phospholipase A2and Arachidonic Acid Release in Cat Iris Sphincter Smooth Muscle Cells

Cited by 12 publications

References 31 publications

Induction by Latanoprost of Collagen Gel Contraction Mediated by Human Tenon Fibroblasts: Role of Intracellular Signaling Molecules

Induction by Latanoprost of Collagen Gel Contraction Mediated by Human Tenon Fibroblasts: Role of Intracellular Signaling Molecules

Endogenous bioactive lipids and the regulation of conventional outflow facility

Stanniocalcin-1 Is an Ocular Hypotensive Agent and a Downstream Effector Molecule That Is Necessary for the Intraocular Pressure–Lowering Effects of Latanoprost

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