ArticleHSOA journal of ophthalmology & clinical research2014
Deletion of SPARC Enhances Retinal Vaso-Obliteration in Mouse Model of Oxygen-Induced Retinopathy.
Article in HSOA journal of ophthalmology & clinical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundSecreted Protein Acidic and Rich in Cysteine (SPARC) is a matricellular protein which is implicated in regulation of angiogenesis. PURPOSE: To characterize the changes in SPARC expression and effect of its deletion in a mouse model Oxygen Induced Retinopathy (OIR). MATERIALS AND
methodsWild type (wt) and SPARC-deficient mice were subjected to high oxygen (75%) for 5 days (p7-p12) before room air for additional 5 days (p12-p17). Retinas from both groups were flat mounted and retinal vessels were labeled with Isolectin-B4. Areas of Retinal Neovascularization (RNV) and vaso-obliteration were measured by Image-J and normalized to total retinal areas. SPARC expression was analyzed in both groups at p14 and p17 in retinal homogenates and sections by Western Blotting (WB) and immunofluorescence respectively. Human Retinal Endothelial Cells (HRECs) were exposed to hypoxia (1% O2) for 6 hours then SPARC was measured in cell lysate and condition medium by WB and ELISA. Moreover, HRECs were treated with VEGF or SPARC to study their mutual regulatory effect.
resultsSPARC-deficient mice demonstrated significant increase in the vaso-obliteration (
conclusionSPARC deletion enhances ischemic retinopathy, thus modulation of SPARC expression could be a novel therapeutic approach to prevent pathological RNV.
Identifiers
26636134PMC4665627W2184274492What OpenQuestion holds
Registered trials
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