scholarly journals Microenvironmental regulation of the sinusoidal endothelial cell phenotype in vitro

Hepatology ◽  
2009 ◽  
Vol 50 (3) ◽  
pp. 920-928 ◽  
Author(s):  
Sandra March ◽  
Elliot E. Hui ◽  
Gregory H. Underhill ◽  
Salman Khetani ◽  
Sangeeta N. Bhatia
Keyword(s):  
Endothelial Cell ◽  
Sinusoidal Endothelial Cell ◽  
Cell Phenotype

scholarly journals Atorvastatin Reduces the Proadhesive and Prothrombotic Endothelial Cell Phenotype Induced by Cocaine and Plasma From Cocaine Consumers In Vitro

2014 ◽  
Vol 34 (11) ◽  
pp. 2439-2448 ◽  
Author(s):  
Claudia G. Sáez ◽  
Karla Pereira-Flores ◽  
Roberto Ebensperger ◽  
Olga Panes ◽  
Teresa Massardo ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Phenotype

1023 Paracrine and autocrine regulation of rat sinusoidal endothelial cell phenotype

Hepatology ◽  
2003 ◽  
Vol 38 ◽  
pp. 649-649
Author(s):  
L DELEVE ◽  
X WANG ◽  
L HU ◽  
M MCCUSKEY ◽  
R MCCUSKEY
Keyword(s):  
Endothelial Cell ◽  
Sinusoidal Endothelial Cell ◽  
Cell Phenotype ◽  
Autocrine Regulation

scholarly journals Long-term exercise training does not alter brachial and femoral artery vasomotor function and endothelial phenotype in healthy pigs

2010 ◽  
Vol 299 (2) ◽  
pp. H379-H385 ◽  
Author(s):  
Jaume Padilla ◽  
Sean C. Newcomer ◽  
Grant H. Simmons ◽  
Kurt V. Kreutzer ◽  
M. Harold Laughlin
Keyword(s):  
Endothelial Cell ◽  
Exercise Training ◽  
Endothelial Function ◽  
Femoral Artery ◽  
Immunoblot Analysis ◽  
Cell Phenotype ◽  
Femoral Arteries ◽  
Vasomotor Function

Although the beneficial effects of exercise training on conduit artery endothelial function are well-established in animals and humans with compromised basal function, whether exercise exerts favorable effects on a healthy endothelium is inconclusive. We sought to determine whether long-term exercise training enhances endothelial function in peripheral conduit arteries of healthy pigs. Using a retrospective analysis of data collected in our laboratory ( n = 127), we compared in vitro brachial and femoral artery endothelium-dependent and -independent relaxation between a group of pigs that exercise-trained for 16–20 wk and a group that remained sedentary. No differences in vasomotor function were found between the 2 groups ( P > 0.05). Additionally, in a subset of pigs ( n = 16), expression levels of 18 proteins that are typically associated with the atherosclerotic process were measured by immunoblot analysis of endothelial cell scrapes obtained from the brachial and femoral arteries. We found no differences ( P > 0.05) in endothelial gene expression between these exercise-trained and sedentary healthy pigs. These results indicate that pigs exhibiting the classic training-induced adaptations do not demonstrate enhanced endothelium-dependent dilation nor reveal a more atheroprotected endothelial cell phenotype in their brachial and femoral arteries than their sedentary but otherwise healthy counterparts.

Carbon monoxide liberated from carbon monoxide-releasing molecule CORM-2 attenuates inflammation in the liver of septic mice

2008 ◽  
Vol 294 (1) ◽  
pp. G184-G191 ◽  
Author(s):  
Gediminas Cepinskas ◽  
Kazuhiro Katada ◽  
Aurelia Bihari ◽  
Richard F. Potter
Keyword(s):  
Carbon Monoxide ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Vascular Endothelial Cell ◽  
Cecal Ligation ◽  
Cell Phenotype ◽  
Vascular Endothelial ◽  
Proinflammatory Responses ◽  
Umbilical Vein Endothelial Cells

Recent studies suggest that exogenously administered CO is beneficial for the resolution of acute inflammation. In this study, we assessed the role of CO liberated from a systemically administered tricarbonyldichlororuthenium-(II)-dimer (CORM-2) on modulation of liver inflammation during sepsis. Polymicrobial sepsis in mice was induced by cecal ligation and perforation (CLP). CORM-2 (8 mg/kg iv) was administered immediately after CLP induction, and neutrophil [polymorphonuclear leukocyte (PMN)] tissue accumulation, activation of transcription factor, NF-κB, and changes in adhesion molecule ICAM-1 expression (inflammation-relevant markers) were assessed in murine liver 24 h later. In addition, the effects and potential mechanisms of CORM-2-released CO in modulation of vascular endothelial cell proinflammatory responses were assessed in vitro. To this end, human umbilical vein endothelial cells (HUVEC) were stimulated with LPS (1 μg/ml) in the presence or absence of CORM-2 (10–100 μM) and production of intracellular reactive oxygen species (ROS), (DHR123 oxidation) and NO (DAF-FM nitrosation) and subsequent activation of NF-κB were assessed 4 h later. In parallel, expression of ICAM-1 and inducible NO synthase (iNOS) proteins along with PMN adhesion to LPS-challenged HUVEC were also assessed. Induction of CLP resulted in increased PMN accumulation, ICAM-1 expression, and activation of NF-κB in the liver of septic mice. These effects were significantly attenuated by systemic administration of CORM-2. In in vitro experiments, CORM-2-released CO attenuated LPS-induced production of ROS and NO, activation of NF-κB, increase in ICAM-1 and iNOS protein expression and PMN adhesion to LPS-stimulated HUVEC. Taken together, these findings indicate that CO released from systemically administered CORM-2 provides anti-inflammatory effects by interfering with NF-κB activation and subsequent downregulation of proadhesive vascular endothelial cell phenotype in the liver of septic mice.

scholarly journals ALK1 as an emerging target for antiangiogenic therapy of cancer

Blood ◽  
2011 ◽  
Vol 117 (26) ◽  
pp. 6999-7006 ◽  
Author(s):  
Sara I. Cunha ◽  
Kristian Pietras
Keyword(s):  
Endothelial Cell ◽  
Antiangiogenic Therapy ◽  
Critical Role ◽  
Tumor Development ◽  
The Body ◽  
Cell Phenotype ◽  
Current View ◽  
Type I

Members of the TGF-β family act on many, if not all, cell types within the body, producing diverse and complex cellular outcomes. Activation of the endothelial cell-restricted TGF-β type I receptor ALK1 results from the binding of several different ligands of the TGF-β family, including bone morphogenetic protein (BMP) 9, BMP10, and TGF-β. Mounting genetic, pharmacologic, and histopathologic evidence supports a critical role for ALK1 signaling in regulation of both developmental and pathologic blood vessel formation. However, the precise function of TGF-β family signaling in endothelial cells is difficult to predict and appears highly context dependent because of the multitude of ligands and receptors influencing the final outcome. Pharmacologic inhibitors of ALK1 have recently been developed and will allow for more accurate studies of ALK1 function in vivo, as well as for assessment of ALK1 as a target for suppression of angiogenesis during tumor development. Herein, we will summarize the current view of ALK1 regulation of endothelial cell phenotype in vitro and in vivo as well as provide an outlook for the ongoing clinical trials of ALK1 inhibitors in malignant disease.

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