The subendothelial extracellular matrix modulates NF-kappaB activation by flow: a potential role in atherosclerosis. - Wikidata - wikimedia - TriplyDB

The subendothelial extracellular matrix modulates NF-kappaB activation by flow: a potential role in atherosclerosis.

The subendothelial extracellular matrix modulates NF-kappaB activation by flow: a potential role in atherosclerosis.

http://www.wikidata.org/entity/Q30436462

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Laminin-10 and Lutheran blood group glycoproteins in adhesion of human endothelial cells Regulated Hyaluronan Synthesis by Vascular Cells Mechanosensitive mechanisms in transcriptional regulation MicroRNAs in flow-dependent vascular remodelling Fibronectin is an important regulator of flow-induced vascular remodeling The Role of TLR2, TLR4, and TLR9 in the Pathogenesis of Atherosclerosis The atypical structure and function of newborn arterial endothelium is mediated by Rho/Rho kinase signaling Altered nitric oxide production mediates matrix-specific PAK2 and NF-κB activation by flow Flow-dependent cellular mechanotransduction in atherosclerosis.The role of p21-activated kinase in the initiation of atherosclerosis.Hemodynamic activation of beta-catenin and T-cell-specific transcription factor signaling in vascular endothelium regulates fibronectin expression.Atheroprone hemodynamics regulate fibronectin deposition to create positive feedback that sustains endothelial inflammation Matrix-specific protein kinase A signaling regulates p21-activated kinase activation by flow in endothelial cells Complex regulation and function of the inflammatory smooth muscle cell phenotype in atherosclerosis Focal adhesion kinase modulates activation of NF-kappaB by flow in endothelial cells.The subendothelial extracellular matrix modulates JNK activation by flow Cell adhesion receptors in mechanotransduction Mapping the dynamics of shear stress-induced structural changes in endothelial cells.The role of cellular adaptation to mechanical forces in atherosclerosis.GRP78 upregulation by atheroprone shear stress via p38-, alpha2beta1-dependent mechanism in endothelial cells.Mechanotransduction in vascular physiology and atherogenesis.p21-activated kinase signaling regulates oxidant-dependent NF-kappa B activation by flow.Endothelial cell PECAM-1 promotes atherosclerotic lesions in areas of disturbed flow in ApoE-deficient mice Matrix-specific suppression of integrin activation in shear stress signaling.Matrix-specific p21-activated kinase activation regulates vascular permeability in atherogenesis.Endothelial cell responses to atheroprone flow are driven by two separate flow components: low time-average shear stress and fluid flow reversal.Localized tensional forces on PECAM-1 elicit a global mechanotransduction response via the integrin-RhoA pathway CD36 deficiency impairs the small intestinal barrier and induces subclinical inflammation in mice.Fibulin-2 and fibulin-5 cooperatively function to form the internal elastic lamina and protect from vascular injury.The arterial microenvironment: the where and why of atherosclerosis.Matricryptic sites control tissue injury responses in the cardiovascular system: relationships to pattern recognition receptor regulated events.Function and mode of regulation of endothelial major histocompatibility complex class II NF-kappaB activity in endothelial cells is modulated by cell substratum interactions and influences chemokine-mediated adhesion of natural killer cells Collagen I matrix turnover is regulated by fibronectin polymerization.α5β1 integrin signaling mediates oxidized low-density lipoprotein-induced inflammation and early atherosclerosis.Sox18 preserves the pulmonary endothelial barrier under conditions of increased shear stress.The gene expression of human endothelial cells is modulated by subendothelial extracellular matrix proteins: short-term response to laminar shear stress.Alternative splicing of endothelial fibronectin is induced by disturbed hemodynamics and protects against hemorrhage of the vessel wall Direct-contact co-culture between smooth muscle and endothelial cells inhibits TNF-alpha-mediated endothelial cell activation.Effects of disturbed flow on vascular endothelium: pathophysiological basis and clinical perspectives

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The subendothelial extracellular matrix modulates NF-kappaB activation by flow: a potential role in atherosclerosis.

http://www.wikidata.org/entity/Q30436462

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2005 թվականի ապրիլին հրատարակված գիտական հոդված

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2005年の論文

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The subendothelial extracellul ...... ntial role in atherosclerosis.

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The subendothelial extracellul ...... ntial role in atherosclerosis.

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The subendothelial extracellul ...... ntial role in atherosclerosis.

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The subendothelial extracellul ...... ntial role in atherosclerosis.

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The subendothelial extracellul ...... ntial role in atherosclerosis.

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The subendothelial extracellul ...... ntial role in atherosclerosis.

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P2093

A Wayne Orr

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Elizabeth Coleman

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Ian J Sarembock

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John M Sanders

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Martin Alexander Schwartz

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Melissa Bevard

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P2860

Atherosclerosis — An Inflammatory Disease

Integrins as receptors for laminins

Alpha 5 beta 1 integrin activates an NF-kappa B-dependent program of gene expression important for angiogenesis and inflammation.

Integrins in mechanotransduction

NF-kappaB: pivotal mediator or innocent bystander in atherogenesis?

Activation of integrins in endothelial cells by fluid shear stress mediates Rho-dependent cytoskeletal alignment

NF-kappaB mediates alphavbeta3 integrin-induced endothelial cell survival

Shaping the nuclear action of NF-kappaB

Adenosine A(2A) receptor stimulation reduces inflammation and neointimal growth in a murine carotid ligation model.

Adhesion molecules and atherogenesis.

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10.1083/JCB.200410073

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1

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169

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7927588

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15809308

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atherosclerosis

extracellular matrix

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2171897

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