Fluorescein leakage of the optic disc in glaucomatous optic neuropathy

Arend, Oliver; Remky, Andreas; Plange, Niklas; Kaup, M.; Schwartz, Bernard

doi:10.1007/s00417-004-1092-7

Cited by 34 publications

(30 citation statements)

References 27 publications

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“…We have shown LC cells produce these proteins in response to TGF-b1, providing good evidence that this cell type may be relevant to ECM metabolism in the ONH, as well as to the fibrotic changes that occur there in POAG. Coexistent with ECM remodeling, the ONH of POAG patients frequently demonstrate increased vascular leakage and hemorrhage, as evidenced by fluorescein fundus angiography and color fundus photography studies (Yamamoto et al, 2004;Arend et al, 2005). In addition to modulation of ECM remodeling enzyme activity and of angiogenesis (Wang and Keiser, 1998;Hoeben et al, 2004), VEGF is a potent inducer of vascular permeability (Behzadian et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Transforming growth factor‐β‐regulated gene transcription and protein expression in human GFAP‐negative lamina cribrosa cells

Kirwan

Leonard

Murphy

et al. 2005

Glia

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Primary open-angle glaucoma (POAG) is a progressive optic neuropathy, which is a major cause of worldwide visual impairment and blindness. Pathological hallmarks of the glaucomatous optic nerve head (ONH) include retinal ganglion cell axon loss and extracellular matrix (ECM) remodeling of the lamina cribrosa layer. Transforming growth factor-beta (TGF-beta) is an important pro-fibrotic modulator of ECM metabolism, whose levels are elevated in human POAG lamina cribrosa tissue compared with non-glaucomatous controls. We hypothesize that in POAG, lamina cribrosa (LC) glial cells respond to elevated TGF-beta, producing a remodeled ONH ECM. Using Affymetrix microarrays, we report the first study examining the effect of TGF-beta1 on global gene expression profiles in glial fibrillary acidic acid (GFAP)-negative LC glial cells in vitro. Prominent among the differentially expressed genes were those with established fibrogenic potential, including CTGF, collagen I, elastin, thrombospondin, decorin, biglycan, and fibromodulin. Independent TaqMan and Sybr Green quantitative PCR analysis significantly validated genes involved in regulation of cell proliferation (platelet-derived growth factor [PDGF-alpha]), angiogenesis (vascular endothelial growth factor [VEGF]), ECM accumulation and degradation (CTGF, IL-11, and ADAMT-S5), and growth factor binding (ESM-1). Bioinformatic analysis of the ESM-1 promoter identified putative Smad and Runx transcription factor binding sites, and luciferase assays confirmed that TGF-beta1 drives transcription of the ESM-1 gene. TGF-beta1 induces expression and release of ECM components in LC cells, which may be important in regulating matrix remodeling in the lamina cribrosa. In disease states such as POAG, the LC cell may represent an important pro-fibrotic cell type and an attractive target for novel therapeutic strategies.

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Section: Discussionmentioning

confidence: 99%

Transforming growth factor‐β‐regulated gene transcription and protein expression in human GFAP‐negative lamina cribrosa cells

Kirwan

Leonard

Murphy

et al. 2005

Glia

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“…Reduction in flow in glaucomatous eyes has been demonstrated specifically in the retrobulbar circulation [12,13,19], the choroidal circulation [14,15,17] and the circulation of the superficial ONH [16][17][18]. Decreased ONH blood flow to specific areas of the neuroretinal rim has been demonstrated to correspond with visual field defects in glaucomatous eyes [18,71,72] and has been purported to be the initial manifestation of the disease [73][74][75][76]. To better understand the literature and the relationship between the various vascular supplies, we provide a brief review of the vascular anatomy of ocular blood flow as it relates to the area of glaucomatous damage, the ONH [11].…”

Section: Nocturnal Hypotensionmentioning

confidence: 99%

Autoregulation of optic nerve head blood flow and its role in open-angle glaucoma

Jones

Kaplowitz

Saeedi

2014

Expert Review of Ophthalmology

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“…The eye and brain have been considered to be immune-privileged sites partly because of the existence of the blood-retinal, blood-brain barrier. However, these barriers are often compromised in injured or diseased retinae and blood vessels become 'leaky' (Arend et al, 2005;Grisanti et al, 1997;Hernandez, 2000). Any transplanted donor cell would then be exposed to immune surveillance by the circulating host lymphocytes (Wekerle et al, 1987).…”

Section: Immune Rejectionmentioning

confidence: 99%

Embryonic stem cells and retinal repair

Vugler

Lawrence

Walsh

et al. 2007

Mechanisms of Development

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In this review we examine the potential of embryonic stem cells (ESCs) for use in the treatment of retinal diseases involving photoreceptors and retinal pigment epithelium (RPE). We outline the ontogenesis of target retinal cell types (RPE, rods and cones) and discuss how an understanding of developmental processes can inform our manipulation of ESCs in vitro. Due to their potential for cellular therapy, special emphasis is placed upon the derivation and culture of human embryonic stem cells (HESCs) and their differentiation towards a retinal phenotype. In terms of achieving this goal, we suggest that much of the success to date reflects permissive in vitro environments provided by established protocols for HESC derivation, propagation and neural differentiation. In addition, we summarise key factors that may be important for enhancing efficiency of retinal cell-type derivation from HESCs. The retina is an amenable component of the central nervous system (CNS) and as such, diseases of this structure provide a realistic target for the application of HESC-derived cellular therapy to the CNS. In order to further this goal, the second component of our review focuses on the cellular and molecular cues within retinal environments that may influence the survival and behaviour of transplanted cells. Our analysis considers both the potential barriers to transplant integration in the retina itself together with the remodelling in host visual centres that is known to accompany retinal dystrophy.

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Fluorescein leakage of the optic disc in glaucomatous optic neuropathy

Cited by 34 publications

References 27 publications

Transforming growth factor‐β‐regulated gene transcription and protein expression in human GFAP‐negative lamina cribrosa cells

Transforming growth factor‐β‐regulated gene transcription and protein expression in human GFAP‐negative lamina cribrosa cells

Autoregulation of optic nerve head blood flow and its role in open-angle glaucoma

Embryonic stem cells and retinal repair

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