Phenotypic Alterations in Senescent Large-Vessel and Microvascular Endothelial Cells

2000 ◽  
Vol 4 (2) ◽  
pp. 117-121 ◽  
Author(s):  
Ugo Cavallaro ◽  
Vera Castelli ◽  
Ugo Del Monte ◽  
Marco R. Soria
Keyword(s):  
Endothelial Cells ◽  
Large Vessel ◽  
Microvascular Endothelial Cells ◽  
Microvascular Endothelial

A PRACTICAL QUESTION BASED ON CROSS-PLATFORM MICROARRAY DATA NORMALIZATION: ARE BOEC MORE LIKE LARGE VESSEL OR MICROVASCULAR ENDOTHELIAL CELLS OR NEITHER OF THEM?

2007 ◽  
Vol 05 (04) ◽  
pp. 875-893 ◽  
Author(s):  
AIXIANG JIANG ◽  
WEI PAN ◽  
LIMING C. MILBAUER ◽  
YU SHYR ◽  
ROBERT P. HEBBEL
Keyword(s):  
Endothelial Cells ◽  
Microarray Data ◽  
Gene List ◽  
Normalization Method ◽  
Large Vessel ◽  
Microvascular Endothelial Cells ◽  
Support Vector ◽  
Cross Platform ◽  
Microvascular Endothelial ◽  
Discriminative Gene

Since the available microarray data of BOEC (human blood outgrowth endothelial cells), large vessel, and microvascular endothelial cells were from two different platforms, a working cross-platform normalization method was needed to make these data comparable. With six HUVEC (human umbilical vein endothelial cells) samples hybridized on two-channel cDNA arrays and six HUVEC samples on Affymetrix arrays, 64 possible combinations of a three-step normalization procedure were investigated to search for the best normalization method, which was selected, based on two criteria measuring the extent to which expression profiles of biological samples of the same cell type arrayed on two platforms were indistinguishable. Next, three discriminative gene lists between the large vessel and the microvascular endothelial cells were achieved by SAM (significant analysis of microarrays), PAM (prediction analysis for microarrays), and a combination of SAM and PAM lists. The final discriminative gene list was selected by SVM (support vector machine). Based on this discriminative gene list, SVM classification analysis with best tuning parameters and 10,000 times of validations showed that BOEC were far from large vessel cells, they either formed their own class, or fell into the microvascular class. Based on all the common genes between the two platforms, SVM analysis further confirmed this conclusion.

Coupling and connexin 43 expression in microvascular and large vessel endothelial cells

1992 ◽  
Vol 262 (5) ◽  
pp. C1246-C1257 ◽  
Author(s):  
M. S. Pepper ◽  
R. Montesano ◽  
A. el Aoumari ◽  
D. Gros ◽  
L. Orci ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Connexin 43 ◽  
Lucifer Yellow ◽  
Large Vessel ◽  
Microvascular Endothelial Cells ◽  
Cx43 Expression ◽  
Endothelial Cell Function ◽  
Junctional Communication ◽  
Cx43 Mrna ◽  
Microvascular Endothelial

Endothelial cells of the microvasculature differ both structurally and functionally from endothelial cells of larger vessels. To assess whether these cells also differ in terms of direct cell-to-cell communication, we compared gap junction-mediated intercellular coupling and connexin (Cx) expression in monolayer cultures of bovine microvascular and large vessel (aortic and pulmonary artery) endothelial cells. In confluent monolayers, junctional communication (as assessed by transfer of Lucifer Yellow) was greater between large vessel than between microvascular endothelial cells. Basal levels of connexin 43 (Cx43) and Cx43 mRNA were also greater in large vessel than in microvascular endothelial cells. When monolayers of microvascular endothelial cells were mechanically wounded, junctional communication was increased between migrating cells at the wound edge. In contrast, coupling between large vessel endothelial cells was not increased after wounding. The wound-induced increase in coupling between microvascular endothelial cells was accompanied by an increase in Cx43 and Cx43 mRNA. In contrast, Cx43 expression was unaltered after wounding monolayers of large vessel endothelial cells. These studies revealed differences in basal and wound-induced levels of coupling and Cx43 expression in microvascular and large vessel endothelial cells in vitro, raising the possibility that the role of coupling in endothelial cell function may be different in these different cell types.

Expression and endocytosis of VEGF and its receptors in human colonic vascular endothelial cells

2002 ◽  
Vol 282 (6) ◽  
pp. G1088-G1096 ◽  
Author(s):  
Dongfang Wang ◽  
Richard E. Lehman ◽  
David B. Donner ◽  
Mary R. Matli ◽  
Robert S. Warren ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Large Vessel ◽  
Microvascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Ulex Europaeus ◽  
Microvascular Endothelial ◽  
Umbilical Vein Endothelial Cells

Normal human colonic microvascular endothelial cells (HUCMEC) have been isolated from surgical specimens by their adherence to Ulex europaeus agglutinin bound to magnetic dynabeads that bind α-l-fucosyl residues on the endothelial cell membrane. Immunocytochemistry demonstrated the presence of a range of endothelial-specific markers on HUCMEC, including the von Willebrand factor, Ulex europaeus agglutinin, and platelet endothelial cell adhesion molecule-1. The growing cells form monolayers with the characteristic cobblestone morphology of endothelial cells and eventually form tube-like structures. HUCMEC produce vascular endothelial growth factor (VEGF) and express the receptors, kinase insert domain-containing receptor (KDR) and fms-like tyrosine kinase, through which VEGF mediates its actions in the endothelium. VEGF induces the tyrosine phosphorylation of KDR and a proliferative response from HUCMEC comparable to that elicited from human umbilical vein endothelial cells (HUVEC). On binding to HUCMEC or HUVEC,125I-labeled VEGF internalizes or dissociates to the medium. Once internalized,125I-labeled VEGF is degraded and no evidence of ligand recycling was observed. However, significantly less VEGF is internalized, and more is released to the medium from HUCMEC than HUVEC. Angiogenesis results from the proliferation and migration of microvascular, not large-vessel, endothelial cells. The demonstration that microvascular endothelial cells degrade less and release more VEGF to the medium than large-vessel endothelial cells identifies a mechanism permissive of the role of microvascular cells in angiogenesis.

Resveratrol Reduces Matrix Metalloproteinase-2 Activity Induced by Oxygen-Glucose Deprivation and Reoxygenation in Human Cerebral Microvascular Endothelial Cells

2012 ◽  
Vol 82 (4) ◽  
pp. 267-274 ◽  
Author(s):  
Zahide Cavdar ◽  
Mehtap Y. Egrilmez ◽  
Zekiye S. Altun ◽  
Nur Arslan ◽  
Nilgun Yener ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Neurovascular Unit ◽  
Glucose Deprivation ◽  
Matrix Metalloproteinase 2 ◽  
Microvascular Endothelial Cells ◽  
Oxygen Glucose Deprivation ◽  
Microvascular Endothelial

The main pathophysiology in cerebral ischemia is the structural alteration in the neurovascular unit, coinciding with neurovascular matrix degradation. Among the human matrix metalloproteinases (MMPs), MMP-2 and -9, known as gelatinases, are the key enzymes for degrading type IV collagen, which is the major component of the basal membrane that surrounds the cerebral blood vessel. In the present study, we investigated the effects of resveratrol on cytotoxicity, reactive oxygen species (ROS), and gelatinases (MMP-2 and -9) in human cerebral microvascular endothelial cells exposed to 6 hours of oxygen-glucose deprivation and a subsequent 24 hours of reoxygenation with glucose (OGD/R), to mimic ischemia/reperfusion in vivo. Lactate dehydrogenase increased significantly, in comparison to that in the normoxia group. ROS was markedly increased in the OGD/R group, compared to normoxia. Correspondingly, ROS was significantly reduced with 50 μM of resveratrol. The proMMP-2 activity in the OGD/R group showed a statistically significant increase from the control cells. Resveratrol preconditioning decreased significantly the proMMP-2 in the cells exposed to OGD/R in comparison to that in the OGD/R group. Our results indicate that resveratrol regulates MMP-2 activity induced by OGD/R via its antioxidant effect, implying a possible mechanism related to the neuroprotective effect of resveratrol.

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