MEF2C ablation in endothelial cells reduces retinal vessel loss and suppresses pathologic retinal neovascularization in oxygen-induced retinopathy (Q36044670)

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English	MEF2C ablation in endothelial cells reduces retinal vessel loss and suppresses pathologic retinal neovascularization in oxygen-induced retinopathy	scientific article

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scholarly article

1 reference

Europe PubMed Central

11 August 2017

MEF2C ablation in endothelial cells reduces retinal vessel loss and suppresses pathologic retinal neovascularization in oxygen-induced retinopathy (English)

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Europe PubMed Central

11 August 2017

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neovascularization

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author name string

Zhenhua Xu

1

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Europe PubMed Central

11 August 2017

Junsong Gong

2

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Europe PubMed Central

11 August 2017

Debasish Maiti

3

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Europe PubMed Central

11 August 2017

Linh Vong

4

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Europe PubMed Central

11 August 2017

Lijuan Wu

5

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Europe PubMed Central

11 August 2017

John J Schwarz

6

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Europe PubMed Central

11 August 2017

Elia J Duh

7

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Europe PubMed Central

11 August 2017

language of work or name

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publication date

19 April 2012

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Europe PubMed Central

11 August 2017

The American Journal of Pathology

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Europe PubMed Central

11 August 2017

180

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Europe PubMed Central

11 August 2017

6

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Europe PubMed Central

11 August 2017

2548-2560

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Europe PubMed Central

11 August 2017

describes a project that uses

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Europe PubMed Central

11 June 2022

https://www.ebi.ac.uk/europepmc/webservices/rest/PMC3378855/fullTextXML

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Reduced retinal neovascularization, vascular permeability, and apoptosis in ischemic retinopathy in the absence of prolyl hydroxylase-1 due to the prevention of hyperoxia-induced vascular obliteration

1 reference

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Novel protective properties of IGFBP-3 result in enhanced pericyte ensheathment, reduced microglial activation, increased microglial apoptosis, and neuronal protection after ischemic retinal injury.

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Ischemic neurons prevent vascular regeneration of neural tissue by secreting semaphorin 3A

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Retinopathy of prematurity: understanding ischemic retinal vasculopathies at an extreme of life

1 reference

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The mouse retina as an angiogenesis model

1 reference

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Phospholipase Cgamma activation drives increased production of autotaxin in endothelial cells and lysophosphatidic acid-dependent regression.

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Norrin promotes vascular regrowth after oxygen-induced retinal vessel loss and suppresses retinopathy in mice.

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Understanding ischemic retinopathies: emerging concepts from oxygen-induced retinopathy.

1 reference

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Quantification of oxygen-induced retinopathy in the mouse: a model of vessel loss, vessel regrowth and pathological angiogenesis

1 reference

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Insulin-like growth factor binding protein-3 mediates vascular repair by enhancing nitric oxide generation

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The effects of oxygen stresses on the development of features of severe retinopathy of prematurity: knowledge from the 50/10 OIR model

1 reference

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A p38 MAPK-MEF2C pathway regulates B-cell proliferation

1 reference

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Effect of heme oxygenase-1 on vascular function and disease

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Transcription factor MEF2C influences neural stem/progenitor cell differentiation and maturation in vivo

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Vascular endothelial growth factor induces MEF2C and MEF2-dependent activity in endothelial cells

1 reference

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Transcription factor Mef2c is required for B cell proliferation and survival after antigen receptor stimulation

1 reference

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Activated NAD(P)H oxidase from supplemental oxygen induces neovascularization independent of VEGF in retinopathy of prematurity model

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Erythropoietin deficiency decreases vascular stability in mice.

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Heme oxygenase-1 and carbon monoxide in vascular pathobiology: focus on angiogenesis

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MEF2: a central regulator of diverse developmental programs

1 reference

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Inhibition of NAD(P)H oxidase reduces apoptosis and avascular retina in an animal model of retinopathy of prematurity

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Increased dietary intake of omega-3-polyunsaturated fatty acids reduces pathological retinal angiogenesis

1 reference

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IGFBP3 suppresses retinopathy through suppression of oxygen-induced vessel loss and promotion of vascular regrowth.

1 reference

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The transcription factor MEF2C is required for craniofacial development

1 reference

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MEF2C is required for the normal allocation of cells between the ventricular and sinoatrial precursors of the primary heart field

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Trans-arachidonic acids generated during nitrative stress induce a thrombospondin-1-dependent microvascular degeneration

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Inhibition of NAD(P)H oxidase activity blocks vascular endothelial growth factor overexpression and neovascularization during ischemic retinopathy.

1 reference

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Inhibition of tumor necrosis factor-alpha improves physiological angiogenesis and reduces pathological neovascularization in ischemic retinopathy.

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Transcription factor Ets-1 mediates ischemia- and vascular endothelial growth factor-dependent retinal neovascularization.

1 reference

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Animal models of oxygen-induced retinopathy

1 reference

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NG2 proteoglycan is expressed exclusively by mural cells during vascular morphogenesis

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SOX18 directly interacts with MEF2C in endothelial cells

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The transcription factor MEF2C-null mouse exhibits complex vascular malformations and reduced cardiac expression of angiopoietin 1 and VEGF

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Requirement of the MADS-box transcription factor MEF2C for vascular development

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Control of mouse cardiac morphogenesis and myogenesis by transcription factor MEF2C

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Thrombospondin-1-deficient mice exhibit increased vascular density during retinal vascular development and are less sensitive to hyperoxia-mediated vessel obliteration

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Oxygen-induced retinopathy in the mouse

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Generation of conditional Mef2cloxP/loxP mice for temporal- and tissue-specific analyses

1 reference

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Sema3A [corrected] resists retinal revascularization

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https://pubmed.ncbi.nlm.nih.gov/22521302

12 December 2020

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10.1016/J.AJPATH.2012.02.021

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Europe PubMed Central

11 August 2017

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Europe PubMed Central

11 August 2017

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Europe PubMed Central

11 August 2017

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