H2O2-induced endothelial NO production contributes to vascular cell apoptosis and increased permeability in rat venules - Wikidata - awgldk - TriplyDB

H2O2-induced endothelial NO production contributes to vascular cell apoptosis and increased permeability in rat venules

H2O2-induced endothelial NO production contributes to vascular cell apoptosis and increased permeability in rat venules

http://www.wikidata.org/entity/Q30532163

about

Acute exertion elicits a H2O2-dependent vasodilator mechanism in the microvasculature of exercise-trained but not sedentary adults.In vitro recapitulation of functional microvessels for the study of endothelial shear response, nitric oxide and [Ca2+]i.Reduced flow-and acetylcholine-induced dilations in visceral compared to subcutaneous adipose arterioles in human morbid obesity.A1 adenosine receptor negatively modulates coronary reactive hyperemia via counteracting A2A-mediated H2O2 production and KATP opening in isolated mouse hearts Wall stretch and thromboxane A₂ activate NO synthase (eNOS) in pulmonary arterial smooth muscle cells via H₂O₂ and Akt-dependent phosphorylation.Development and Characterization of In Vitro Microvessel Network and Quantitative Measurements of Endothelial [Ca2+]i and Nitric Oxide Production.New insights into shear stress-induced endothelial signalling and barrier function: cell-free fluid versus blood flow.

P2860

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P2860

H2O2-induced endothelial NO production contributes to vascular cell apoptosis and increased permeability in rat venules

http://www.wikidata.org/entity/Q30532163

description

2012 nî lūn-bûn

@nan

2012 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2012 թվականի հոտեմբերին հրատարակված գիտական հոդված

@hy

2012年の論文

@ja

2012年論文

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2012年論文

@zh-hant

2012年論文

@zh-hk

2012年論文

@zh-mo

2012年論文

@zh-tw

2012年论文

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name

H2O2-induced endothelial NO pr ...... ed permeability in rat venules

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H2O2-induced endothelial NO pr ...... ed permeability in rat venules

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type

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H2O2-induced endothelial NO pr ...... ed permeability in rat venules

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H2O2-induced endothelial NO pr ...... ed permeability in rat venules

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prefLabel

H2O2-induced endothelial NO pr ...... ed permeability in rat venules

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H2O2-induced endothelial NO pr ...... ed permeability in rat venules

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AJPHEART.00300.2012

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American Journal of Physiology - Heart and Circulatory Physiology

P1476

H2O2-induced endothelial NO pr ...... ed permeability in rat venules

@en

P2093

Dong Yuan

http://www.w3.org/2001/XMLSchema#string

Mingxia Wang

http://www.w3.org/2001/XMLSchema#string

Pingnian He

http://www.w3.org/2001/XMLSchema#string

Xueping Zhou

http://www.w3.org/2001/XMLSchema#string

P2860

Signal transduction of eNOS activation

Direct interaction of endothelial nitric-oxide synthase and caveolin-1 inhibits synthase activity

Vascular remodeling alters adhesion protein and cytoskeleton reactions to inflammatory stimuli resulting in enhanced permeability increases in rat venules.

Temporal and spatial correlation of platelet-activating factor-induced increases in endothelial [Ca²⁺]i, nitric oxide, and gap formation in intact venules

Endothelial [Ca2+]i and caveolin-1 antagonistically regulate eNOS activity and microvessel permeability in rat venules

The Akt kinase signals directly to endothelial nitric oxide synthase

Interaction between caveolin-1 and the reductase domain of endothelial nitric-oxide synthase. Consequences for catalysis

The biochemistry of apoptosis

Endothelial dysfunction in cardiovascular diseases: the role of oxidant stress

Differential arterial/venous expression of NG2 proteoglycan in perivascular cells along microvessels: identifying a venule-specific phenotype.

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H82-93

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10.1152/AJPHEART.00300.2012

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1

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304

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