Thrombin-Induced Platelet Adhesion to Endothelial Cells in Culture and under Flow Conditions: Role of Endothelium-Derived Nitric Oxide and Prostacyclin1

2015 ◽  
pp. 315-324
Author(s):  
Catherine M. Venturini ◽  
Fred L. Minnear ◽  
Peter J. Del Vecchio ◽  
John W. Fenton ◽  
John E. Kaplan
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Platelet Adhesion ◽  
Flow Conditions ◽  
Cells In Culture

scholarly journals Permissive Role of Nitric Oxide in Endothelin-induced Migration of Endothelial Cells

1997 ◽  
Vol 272 (3) ◽  
pp. 1747-1752 ◽  
Author(s):  
Eisei Noiri ◽  
Yu Hu ◽  
Wadie F. Bahou ◽  
Charles R. Keese ◽  
Ivar Giaever ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Permissive Role

Discovery of Side- and Shear-Dependent miRNAs and mRNAs in Human Aortic Valvular Endothelial Cells

2011 ◽  
Author(s):  
Casey J. Holliday ◽  
Randall F. Ankeny ◽  
Hanjoong Jo ◽  
Robert M. Nerem
Keyword(s):  
Endothelial Cells ◽  
Aortic Valve ◽  
Oscillatory Flow ◽  
Expression Profiles ◽  
Flow Conditions ◽  
Expression Of Genes ◽  
Inflammatory Phenotype ◽  
Cardiovascular Pathologies ◽  
Laminar Shear

Aortic valve (AV) disease is diagnosed by severe symptoms, such as calcification, and typically treated by AV replacement and repair surgeries. The mechanism by which AV disease occurs, specifically the role of the endothelium remains relatively unknown. It is known that disease preferentially occurs on the fibrosa, or aortic side, where it is exposed to disturbed, oscillatory flow, whereas the ventricularis, or side facing the left ventricle, experiences pulsatile, laminar shear and remains non-calcified [1, 2]. Research shows that regulation of miRNAs, short nucleotide segments targeting mRNAs, coincides with cardiovascular pathologies [3] though expression profiles of miRNAs and the mRNAs they modulate in human AV endothelial cells (HAVECs) have not been reported. We hypothesize that disturbed flow conditions present on the fibrosa stimulate ECs to modify expression of genes and miRNAs to induce a pro-inflammatory phenotype.

The role of nitric oxide and cGMP in platelet adhesion to vascular endothelium

1987 ◽  
Vol 148 (3) ◽  
pp. 1482-1489 ◽  
Author(s):  
Marek W. Radomski ◽  
Richard M.J. Palmer ◽  
Salvador Moncada
Keyword(s):  
Nitric Oxide ◽  
Vascular Endothelium ◽  
Platelet Adhesion

scholarly journals Role of endothelial nitric oxide synthase-derived nitric oxide in activation and dysfunction of cerebrovascular endothelial cells during early onsets of sepsis

2008 ◽  
Vol 295 (4) ◽  
pp. H1712-H1719 ◽  
Author(s):  
Osamu Handa ◽  
Jancy Stephen ◽  
Gediminas Cepinskas
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Nitric Oxide Synthase ◽  
Mass Flux ◽  
Oxidant Stress ◽  
Junction Protein ◽  
Cerebrovascular Endothelial Cells ◽  
Oxide Synthase ◽  
The Brain

Sepsis-associated encephalopathy is an early manifestation of sepsis, resulting in a diffuse dysfunction of the brain. Recently, nitric oxide (NO) has been proposed to be one of the key molecules involved in the modulation of inflammatory responses in the brain. The aim of this study was to assess the role of NO in cerebrovascular endothelial cell activation/dysfunction during the early onsets of sepsis. To this end, we employed an in vitro model of sepsis in which cultured mouse cerebrovascular endothelial cells (MCVEC) were challenged with blood plasma (20% vol/vol) obtained from sham or septic (feces-induced peritonitis, FIP; 6 h) mice. Exposing MCVEC to FIP plasma for 1 h resulted in increased production of reactive oxygen species and NO as assessed by intracellular oxidation of oxidant-sensitive fluorochrome, dihydrorhodamine 123 (DHR 123), and nitrosation of NO-specific probe, DAF-FM, respectively. The latter events were accompanied by dissociation of tight junction protein, occludin, from MCVEC cytoskeletal framework and a subsequent increase in FITC-dextran (3-kDa mol mass) flux across MCVEC grown on the permeable cell culture supports, whereas Evans blue-BSA (65-kDa mol mass) or FITC-dextran (10-kDa mol mass) flux were not affected. FIP plasma-induced oxidant stress, occludin rearrangement, and MCVEC permeability were effectively attenuated by antioxidant, 1-pyrrolidinecarbodithioic acid (PDTC; 0.5 mM), or interfering with nitric oxide synthase (NOS) activity [0.1 mM nitro-l-arginine methyl ester (l-NAME) or endothelial NOS (eNOS)-deficient MCVEC]. However, treatment of MCVEC with PDTC failed to interfere with NO production, suggesting that septic plasma-induced oxidant stress in MCVEC is primarily a NO-dependent event. Taken together, these data indicate that during early sepsis, eNOS-derived NO exhibits proinflammatory characteristics and contributes to the activation and dysfunction of cerebrovascular endothelial cells.

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