Proteoglycans in the Eye

Tanihara, Hidenobu; Inatani, Masaru; Koga, Toshikatsu; Yano, Tsuyoshi; Kimura, Akira

doi:10.1097/01.ico.0000263121.45898.d2

Cited by 48 publications

(32 citation statements)

References 19 publications

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“…In addition to HA, stabilin-2 has been shown to bind and clear proteoglycans such as chondroitin sulfate proteoglycan, and serglycin from the circulation (Smedsrød et al 1985;Øynebråten et al 2000). HA and proteoglycans are highly expressed in ocular tissues, where they, for example, contribute to the stromal transparency of the cornea (Tanihara et al 2002). The cornea consists of a stromal layer, which is covered at its external surface by epithelium in contact with tear fluid, and at its inner surface by an endothelium in contact with aqueous fluid in the anterior chamber.…”

Section: Discussionmentioning

confidence: 98%

Expression of stabilin-2, a novel fasciclin-like hyaluronan receptor protein, in murine sinusoidal endothelia, avascular tissues, and at solid/liquid interfaces

Falkowski

Schledzewski

Hansen

et al. 2003

Histochemistry and Cell Biology

127

143

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Stabilin-2, the hepatic hyaluronan receptor, has recently been cloned by us. Together with stabilin-1, stabilin-2 constitutes a novel family of fasciclin-like hyaluronan receptor homologues. Here, we analyzed expression of stabilin-2 (mStab-2) in a broad array of C57BL/6 mouse organs and tissues. While northern blot analysis showed positive expression of mStab-2 mRNA confined to liver and spleen, immunohistochemistry demonstrated mStab-2 protein expression in the endothelial sinuses of liver, lymph nodes, spleen, and bone marrow, and in specialized structures of eye, heart, brain, and kidney. Expression of mStab-2 was detected in corneal and lens epithelium, in mesenchymal cells of the heart valves, in the ependymal cells lining the ventricles in the brain, and in the prismatic epithelial cells covering the renal papillae. In pathological conditions, such as tumor growth or wound healing processes, mStab-2 was not expressed in the newly formed vasculature or other tissue components. Based on these results, we suggest that mStab-2 might be involved in the clearance of hyaluronan from the lymph or the blood circulation via the network of endothelial sinuses. At the other mStab-2-positive tissues sites that are either avascular and/or demarcate a solid/liquid interface, mStab-2 may serve to maintain tissue integrity by supporting extracellular matrix turnover or it may contribute to maintaining fluidity of bodily liquids by resorption of hyaluronan.

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Section: Discussionmentioning

confidence: 98%

Expression of stabilin-2, a novel fasciclin-like hyaluronan receptor protein, in murine sinusoidal endothelia, avascular tissues, and at solid/liquid interfaces

Falkowski

Schledzewski

Hansen

et al. 2003

Histochemistry and Cell Biology

127

143

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“…The keratocyte hallmarks, dendritic morphology, keratocan expression and KS production, are rapidly lost, reduced or altered in serum culture. Fibroblastic cells, in contrast, adopt elongated cell bodies and secrete biglycan and type III collagen, matrix components that are absent from healthy stroma but present in opaque scar tissues [20,30,31]. In hydrogel constructs, RT-PCR and confocal imaging indicated the production of normal stromal matrix components, particularly when primary and P1 cells are encapsulated.…”

Section: Discussionmentioning

confidence: 99%

Keratocyte behavior in three-dimensional photopolymerizable poly(ethylene glycol) hydrogels

et al. 2008

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The goal of this study was to evaluate three-dimensional (3-D) poly(ethylene glycol) (PEG) hydrogels as a culture system for studying corneal keratocytes. Bovine keratocytes were subcultured in DMEM/F-12 containing 10% fetal bovine serum (FBS) through passage 5. Primary keratocytes (P0) and corneal fibroblasts from passages 1 (P1) and 3 (P3) were photoencapsulated at various cell concentrations in PEG hydrogels via brief exposure to light. Additional hydrogels contained adhesive YRGDS and nonadhesive YRDGS peptides. Hydrogel constructs were cultured in DMEM/F-12 with 10% FBS for 2 and 4 weeks. Cell viability was assessed by DNA quantification and vital staining. Biglycan, type I collagen, type III collagen, keratocan and lumican expression were determined by reverse transcriptase-polymerase chain reaction. Deposition of type I collagen, type III collagen and keratan sulfate (KS)-containing matrix components was visualized using confocal microscopy. Keratocytes in a monolayer lost their stellate morphology and keratocan expression, displayed elongated cell bodies, and up-regulated biglycan, type I collagen and type III collagen characteristic of corneal fibroblasts. Encapsulated keratocytes remained viable for 4 weeks with spherical morphologies. Hydrogels supported production of KS, type I collagen and type III collagen matrix components. PEG-based hydrogels can support keratocyte viability and matrix production. 3-D hydrogel culture can stabilize but not restore the keratocyte phenotype. This novel application of PEG hydrogels has potential use in the study of corneal keratocytes in a 3-D environment.

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“…This indicates that in glaucoma, the site of increased outflow resistance lies proximal to the collector channels, ruling out distal outflow pathway tissues as potential therapeutic targets [65,68,70]. It is generally accepted that the majority of outflow resistance is generated at the JCT [42,66], in particular, at the ECM of the JCT [34,[71][72][73]. Porous spaces within the ECM of this region allow AH to reach the endothelial lining of SC; however, proteoglycans, glycosaminoglycans, and other large ECM constituents can fill these spaces further increasing resistance to AH outflow [42,[74][75][76][77].…”

Section: Ecm In Outflow Resistancementioning

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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Proteoglycans in the Eye

Cited by 48 publications

References 19 publications

Expression of stabilin-2, a novel fasciclin-like hyaluronan receptor protein, in murine sinusoidal endothelia, avascular tissues, and at solid/liquid interfaces

Expression of stabilin-2, a novel fasciclin-like hyaluronan receptor protein, in murine sinusoidal endothelia, avascular tissues, and at solid/liquid interfaces

Keratocyte behavior in three-dimensional photopolymerizable poly(ethylene glycol) hydrogels

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

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