1
40
2
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
n/a
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1880-1892
Issue
204
Volume
16
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Suppression of transforming growth factor-beta effects in rabbit subconjunctival fibroblasts by activin receptor-like kinase 5 inhibitor
Publisher
An entity responsible for making the resource available
Molecular Vision
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-09
Subject
The topic of the resource
anti-scarring agent; Biochemistry & Molecular Biology; choroidal; extracellular-matrix; fibrosis; glaucoma; identification; in-vivo; mitomycin-c; neovascularization; Ophthalmology; Surgery; tgf-beta
Creator
An entity primarily responsible for making the resource
Sapitro J; Dunmire J J; Scott S E; Sutariya V; Geldenhuys W J; Hewit M; Yue Byjt; Nakamura H
Description
An account of the resource
Purpose: Transforming growth factor-beta (TGF-beta) activity has been implicated in subconjunctival scarring in eyes following glaucoma filtration surgery (GFS). The purpose of this study is to determine whether an inhibitor for activin receptor-like kinase (ALK) 5 (also known as TGF-beta receptor type I) could suppress TGF-beta activity and thereby promote filtering bleb survival after GFS in a rabbit model. Methods: An ALK-5 inhibitor, SB-505124, was used. A docking study was performed to investigate the interaction between the inhibitor and the receptor. Immunofluorescence for connective tissue growth factor (CTGF) and alpha-smooth muscle actin (alpha-SMA) was performed in cultured rabbit subconjunctival fibroblasts. Immunoblotting for phosphorylated Smad2 (pSmad2), CTGF, and alpha-SMA was also performed. In an in vivo rabbit GFS model, SB-505124 was delivered in a lactose tablet during surgery. Eyes were examined by slit-lamp and intraocular pressure (IOP) was measured until the time of bleb failure or up to 28 days after surgery. Tissue sections on day 5 after surgery were histologically evaluated after staining with hematoxylin and eosin. The sections were also immunostained for CTGF and alpha-SMA. In addition, cell outgrowth from dissected subconjunctival tissues placed in a cell culture flask with media was investigated. Results: The docking study indicated hydrogen bond interactions between SB-505124 and amino acids His-283 and Ser-280 ALK-5. Suppression of pSmad2, CTGF, and alpha-SMA by SB-505124 was observed in cultured fibroblasts. Filtering blebs in the GFS with SB-505124 group were maintained for more than 10 days, and the period of bleb survival was significantly longer than that in controls. IOP levels after surgery seemed to be related to bleb survival. Histologically, subconjunctival cell infiltration and scarring at the surgical site in the GFS with SB-505124 and mitomycin C (MMC) groups were much subsided compared to controls. Suppression of CTGF and alpha-SMA by SB-505124 was also observed by immunofluorescence. Cell outgrowth from explants dissected from eyes to which SB-505124 was applied during GFS was robust while outgrowth was poor from those treated with MMC. Conclusions: The ALK-5 inhibitor SB-505124 was efficacious both in vitro and in vivo in suppressing the TGF-beta action. The inhibitor may provide a novel therapy for preventing ocular inflammation and scarring.
Identifier
An unambiguous reference to the resource within a given context
n/a
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2010
anti-scarring agent
Biochemistry & Molecular Biology
choroidal
Dunmire J J
extracellular-matrix
Fibrosis
Geldenhuys W J
Glaucoma
Hewit M
identification
in-vivo
Journal Article
mitomycin-c
Molecular Vision
Nakamura H
Neovascularization
Ophthalmology
Sapitro J
Scott S E
Surgery
Sutariya V
tgf-beta
Yue Byjt
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
n/a
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
2492-2498
Issue
283
Volume
14
Search for Full-text
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<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Human anterior chamber angle development without cell death or macrophage involvement
Publisher
An entity responsible for making the resource available
Molecular Vision
Date
A point or period of time associated with an event in the lifecycle of the resource
2008
2008-12
Subject
The topic of the resource
Ophthalmology; Biochemistry & Molecular Biology; light; aqueous outflow system; human eye; human trabecular meshwork; iridocorneal angle
Creator
An entity primarily responsible for making the resource
Meghpara B; Li X; Nakamura H; Khan A; Bejjani B A; Lin S; Edward D P
Description
An account of the resource
Purpose: The iridocorneal angle in the mammalian eye including the trabecular meshwork (TM) develops from undifferentiated mesenchyme/neural crest between the iris root and cornea. The precise mechanisms underlying anterior angle development are unclear, and the contribution of cell death and phagocytic resorption by macrophages in angle development is controversial. In this study, we examined the human anterior chamber angle during various stages of development for evidence of cell death and phagocytic resorption. Methods: Eyes from the human fetus (F) of 7, 8, 9, 10, 11, 13, 15, 18, 19, 21, 22, 23, and 27 weeks as well as eyes from 5-and 11-month-old children and donors 24, 48, and 67 years of age were obtained. Formalin-fixed and paraffin-embedded sections were examined by hematoxylin and eosin (H&E) staining. Immunohistochemistry was performed using polyclonal antibodies against CD68. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) labeling was also performed to evaluate cell death. Results: By light microscopy, the development of human angle structures appeared to progress as previously described. Histological evidence of cellular death or resorption by macrophages was not observed. Furthermore, the chamber angle tissues did not stain with CD68 at any stage of development. Few CD68 positive cells were observed in the iris stroma and the anterior ciliary body between fetal weeks 10 and 18 (F10w and F18w). TUNEL labeled nuclei were not detected in the anterior chamber angle in any fetal or infant eyes. By contrast, TUNEL positive nuclei in TM cells were observed in the examined adult donor specimens. Conclusions: The results suggest that at the time points examined, neither cell death nor phagocytic resorption with macrophages appear to play a role in the development of the human anterior chamber angle.
Identifier
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n/a
Format
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Journal Article or Conference Abstract Publication
2008
aqueous outflow system
Bejjani B A
Biochemistry & Molecular Biology
Edward D P
human eye
human trabecular meshwork
iridocorneal angle
Journal Article or Conference Abstract Publication
Khan A
Li X
Light
Lin S
Meghpara B
Molecular Vision
Nakamura H
Ophthalmology