2012
DOI: 10.1152/japplphysiol.00102.2012
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Vascular remodeling alters adhesion protein and cytoskeleton reactions to inflammatory stimuli resulting in enhanced permeability increases in rat venules

Abstract: Yuan D, He P. Vascular remodeling alters adhesion protein and cytoskeleton reactions to inflammatory stimuli resulting in enhanced permeability increases in rat venules.

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Cited by 22 publications
(23 citation statements)
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References 37 publications
(49 reference statements)
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“…Lipopolysaccharide (LPS), the bacterial endotoxin and an outer membrane component, induces proinflammatory cytokines, adhesion molecules, endothelial permeability changes, and apoptosis regulated by TLR-4 signaling via activation of Rho GTPase-dependent signaling cascade, NF-B activation, and rearrangement of cytoskeletal proteins (15, 31). Despite recent advances in understanding the pathogenesis of ALI/ARDS, effective pharmacological therapies are not currently available and the molecular mechanisms regulating endothelial barrier dysfunction in ALI/ARDS are not completely defined.Interactions between focal adhesions, extracellular matrix, and cytoskeletal proteins have been implicated in endothelial cell (EC) remodeling and barrier dysfunction associated with LPS-and ventilator-induced lung injury (15,31,48). Specific posttranslational modifications such as phosphorylation of focal adhesion proteins are also known to play a role in endothelial barrier regulation to agonists and endotoxin (8, 31).…”
mentioning
confidence: 99%
See 1 more Smart Citation
“…Lipopolysaccharide (LPS), the bacterial endotoxin and an outer membrane component, induces proinflammatory cytokines, adhesion molecules, endothelial permeability changes, and apoptosis regulated by TLR-4 signaling via activation of Rho GTPase-dependent signaling cascade, NF-B activation, and rearrangement of cytoskeletal proteins (15, 31). Despite recent advances in understanding the pathogenesis of ALI/ARDS, effective pharmacological therapies are not currently available and the molecular mechanisms regulating endothelial barrier dysfunction in ALI/ARDS are not completely defined.Interactions between focal adhesions, extracellular matrix, and cytoskeletal proteins have been implicated in endothelial cell (EC) remodeling and barrier dysfunction associated with LPS-and ventilator-induced lung injury (15,31,48). Specific posttranslational modifications such as phosphorylation of focal adhesion proteins are also known to play a role in endothelial barrier regulation to agonists and endotoxin (8, 31).…”
mentioning
confidence: 99%
“…Interactions between focal adhesions, extracellular matrix, and cytoskeletal proteins have been implicated in endothelial cell (EC) remodeling and barrier dysfunction associated with LPS-and ventilator-induced lung injury (15,31,48). Specific posttranslational modifications such as phosphorylation of focal adhesion proteins are also known to play a role in endothelial barrier regulation to agonists and endotoxin (8, 31).…”
mentioning
confidence: 99%
“…It could involve structural alterations in the vascular walls including the changes in size and cellular compositions. Currently, most of the vascular remodelling studies focus on large arteries and arterioles but only a few have investigated remodelling in microvessels, a site that allows macromolecules to escape, resulting in tissue oedema and organ dysfunction (Yuan and He, 2012). We have previously reported vascular modelling in the specific sites of the retinal vein, arteriovenous crossing and laminar cribrosa region where risk sites for retinal vein occlusion are present (Kang et al, 2011(Kang et al, , 2013Yu et al, 2014;Yu et al, 2012).…”
Section: Discussionmentioning
confidence: 99%
“…While early investigations used frog microvessels in mesentery and thin cutaneous pectoris muscle 7,8 , by far the most commonly used preparation in mammalian models is the rat mesentery [9][10][11][12][13][14][15] . Most investigations have focused on acute changes in vascular permeability studied over periods of 1-4 hr, but more recent investigations have been extended to measurements on individual vessels 24-72 hr after an initial perfusion [18][19][20][21][22][23][24][25][26] The fundamental aspect of the technique is the measurement of volume flow (J v ) across a defined surface area (S) of the microvessel wall.…”
Section: Introductionmentioning
confidence: 99%
“…Measurement of transvascular flows may also be combined with more detailed investigations using a sophisticated fluorescence microscope with appropriate filters such as rigs used for measurements of solute permeability, fluorescent ratio monitoring of cytoplasmic calcium or other cellular mechanisms, and confocal imaging 6,12,13,27 . A key advantage of all microperfusion approaches is the ability to make repeated measures, on the same vessel, under controlled change of driving force such as hydrostatic and oncotic pressures, or induced change in vessel responses to inflammatory conditions.…”
Section: Introductionmentioning
confidence: 99%