Endothelin-like immunoreactivity in aqueous humor of patients with primary open-angle glaucoma and cataract

Noske, W; Hensen, J.; Wiederholt, Michael

doi:10.1007/bf00947082

Cited by 155 publications

(82 citation statements)

References 4 publications

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“…33,[40][41][42][43] These apparent alterations in the circulation of the glaucomatous optic nerve may implicate dysfunction of vascular regulatory mechanisms. Further support for vascular dysregulation has been suggested by the finding of elevation of ET-1, a potent vasoconstricting peptide, in the plasma 39,[44][45][46] and aqueous humor 47,48 of patients with glaucoma. In the optic nerve, evidence of decreased blood flow correlating with visual field damage has been reported in glaucoma patients.…”

Section: Glaucoma and Systemic Vascular Diseasementioning

confidence: 97%

“…86 In some individuals with primary open-angle glaucoma, higher-thannormal plasma and aqueous humor concentrations of E-1 have been observed. 44,45,47,87 This high concentration of E-1 has been associated with reduced blood flow in the posterior ciliary arteries that supply the optic nerve vasculature. 39 Normal peripheral vascular response to the E-1 is also altered in some individuals with glaucoma.…”

Section: Endothelial Factors (Endothelins)mentioning

confidence: 99%

“…[138][139][140][141] This concept may be particularly interesting because patients with primary open-angle glaucoma may have higher ET-1 levels in the plasma and vitreous humor, as compared to normal controls. 39,44,45,47,48 Thus, ET-1 may cause blood flow insufficiencies in the optic nerve due to its potent vasoconstrictive effect or, on the other hand, may cause neuronal damage mediated by ET b receptors on the glial cells via mechanisms not yet fully understood. This also provides the potential opportunity of developing therapeutic approaches for the treatment of glaucoma, via blockade of endothelin activity or otherwise enhancing the blood flow to the anterior optic nerve.…”

mentioning

confidence: 99%

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Ischemic model of optic nerve injury

Cioffi

2006

American Journal of Ophthalmology

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Section: Glaucoma and Systemic Vascular Diseasementioning

confidence: 97%

Section: Endothelial Factors (Endothelins)mentioning

confidence: 99%

mentioning

confidence: 99%

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Ischemic model of optic nerve injury

Cioffi

2006

American Journal of Ophthalmology

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“…[23][24][25][26][27][28] A great deal of effort has gone into exploring how these different bioactive agents influence TM tissue properties and cell biology in the context of AH outflow in both in vitro and in vivo studies. 15,16,24,[29][30][31][32][33][34][35][36] These efforts are beginning to unravel the participation of several different intracellular signaling mechanisms, including Rho GTPase, Wnt, ECM/ mechanotransduction, integrins, nitric oxide, PKC, BMPs/ SMADs, MAP kinases, and others, in regulating contractile properties of TM cells, ECM turnover, adhesive interactions, biomechanical properties, permeability, and survival of outflow pathway tissues and cells.…”

Section: Introductionmentioning

confidence: 99%

Bioactive Lysophospholipids: Role in Regulation of Aqueous Humor Outflow and Intraocular Pressure in the Context of Pathobiology and Therapy of Glaucoma

Rao

2014

Journal of Ocular Pharmacology and Therapeutics

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Homeostasis of aqueous humor (AH) outflow and intraocular pressure (IOP) is essential for normal vision. Impaired AH outflow through the trabecular meshwork (TM) and a resultant elevation in IOP are common changes in primary open-angle glaucoma (POAG), which is the most prevalent form of glaucoma. Although elevated IOP has been recognized as a definitive risk factor for POAG and lowering elevated IOP remains a mainstay for glaucoma treatment, little is known about the molecular mechanisms, especially external cues and intracellular pathways, involved in the regulation of AH outflow in both normal and glaucomatous eyes. In addition, despite the recognition that increased resistance to AH outflow via the conventional pathway consisting of TM and Schlemm's canal is the main cause for elevated IOP, there are no clinically approved drugs that target the conventional pathway to lower IOP in glaucoma patients. The aim of this article is to briefly review published work on the importance of bioactive lysophospholipids (eg, lysophosphatidic acid and sphingosine-1-phosphate), their receptors, metabolism, signaling, and role in the regulation of AH outflow via the TM and IOP, and to discuss pharmacological targeting of key proteins in the lysophospholipid signaling pathways to lower IOP in glaucoma patients.

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“…POAG subjects have significantly higher levels of ET-1 in plasma and aqueous humor compared to their age matched controls (Sugiyama et al, 1995 andNoske et al, 1997). Animal models of glaucoma with elevated IOP also demonstrate significant increase in ET-1 levels (Kallberg et al, 2002;Prasanna et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Endothelin-1 mediated regulation of extracellular matrix collagens in cells of human lamina cribrosa

Rao

Krishnamoorthy

Yorio

2008

Experimental Eye Research

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Endothelin-1(ET-1), a potent vaso-active peptide, mediates extracellular matrix regulation resulting in an increase in collagen deposition in various cell types and tissues and has been proposed to play a key role in glaucoma pathology. The role of ET-1 in the regulation of extracellular matrix collagens at the level of optic nerve head is not known. In this study we have examined the role of ET-1 in extracellular matrix collagen regulation in primary cultures of human lamina cribrosa cells. Our hypothesis is that ET-1 increases remodeling of the ECM of cells of the lamina cribrosa. Such actions could contribute to the development of optic neuropathy. QPCR analysis revealed that ET-1 mediated an increase in mRNA levels of collagen type I alpha 1 and collagen type VI alpha 1 chains at all doses of ET-1 with a significant increase at 1nM and 10nM concentration in LC cells. A dose dependent increase in collagen type I and type VI protein deposition and secretion was also observed by Western blot in response to ET-1 and was significant at 10nM and 100nM concentrations of ET-1. ET-1 increased the [ 3 H] proline uptake in LC cells suggesting that ET-1 contributed to an increase in total collagen synthesis in LC cells. ET-1 -mediated increase in collagen type I, type VI and total collagen synthesis was significantly blocked by the ET A receptor antagonist, BQ610, as well as with the ET B receptor antagonist, BQ788, suggesting the involvement of both receptor subtypes in ET-1 mediated collagen synthesis in LC cells. These results suggest that ET-1 regulates extra cellular matrix-collagen synthesis in LC cells and may contribute to ECM remodeling at the level of LC of POAG subjects who have elevated plasma and aqueous humor levels of endothelin-1.

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Endothelin-like immunoreactivity in aqueous humor of patients with primary open-angle glaucoma and cataract

Abstract: This finding may indicate a role of ET in POAG or ocular antihypertensive treatment, and its relevance should be further investigated.

Cited by 155 publications

References 4 publications

Ischemic model of optic nerve injury

Ischemic model of optic nerve injury

Bioactive Lysophospholipids: Role in Regulation of Aqueous Humor Outflow and Intraocular Pressure in the Context of Pathobiology and Therapy of Glaucoma

Endothelin-1 mediated regulation of extracellular matrix collagens in cells of human lamina cribrosa

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