scholarly journals Circulating endothelial cells: life, death, detachment and repair of the endothelial cell layer

2002 ◽  
Vol 17 (10) ◽  
pp. 1728-1730 ◽  
Author(s):  
A. Woywodt
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Layer ◽  
Circulating Endothelial Cells ◽  
Endothelial Cell Layer

scholarly journals The Role of PPARs in the Endothelium: Implications for Cancer Therapy

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-12 ◽  
Author(s):  
David Bishop-Bailey ◽  
Karen E. Swales
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Platelet Activation ◽  
Inflammatory Cell ◽  
Cell Layer ◽  
Cell Recruitment ◽  
Blood Vessel Formation ◽  
Endothelial Cell Layer ◽  
Inflammatory Cell Recruitment

The growth and metastasis of cancers intimately involve the vasculature and in particular the endothelial cell layer. Tumours require new blood vessel formation via angiogenesis to support growth. In addition, inflammation, coagulation, and platelet activation are common signals in the growth and metastasis of tumour cells. The endothelium plays a central role in the homeostatic control of inflammatory cell recruitment, regulating platelet activation and coagulation pathways. PPAR, -/, and - are all expressed in endothelial cells. This review will discuss the roles of PPARs in endothelial cells in relation to angiogenesis, inflammation, coagulation, and platelet control pathways. In particular, we will discuss the recent evidence that supports the hypothesis that PPAR and PPAR are antiangiogenic receptors, while PPAR/ is proangiogenic.

Plasmin-induced reduction of heparan sulfate in cultured vascular endothelial cell layer

1994 ◽  
Vol 74 (2) ◽  
pp. 85-93 ◽  
Author(s):  
Toshiyuki Kaji ◽  
Syouichi Hiraga ◽  
Noriyasu Fujii ◽  
Chika Yamamoto ◽  
Michiko Sakamoto ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Heparan Sulfate ◽  
Cell Layer ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Endothelial Cell Layer

scholarly journals Endothelial Cell Layer Subjected to Impinging Flow Mimicking the Apex of an Arterial Bifurcation

2008 ◽  
Vol 36 (10) ◽  
pp. 1681-1689 ◽  
Author(s):  
Michael P. Szymanski ◽  
Eleni Metaxa ◽  
Hui Meng ◽  
John Kolega
Keyword(s):  
Endothelial Cell ◽  
Cell Layer ◽  
Arterial Bifurcation ◽  
Endothelial Cell Layer ◽  
Impinging Flow

Necklace-like detachment of endothelial cell layer from arterial wall under low-calcium condition

1994 ◽  
Vol 46 (4-5) ◽  
pp. 307-313 ◽  
Author(s):  
Hisao Yamaguchi ◽  
Masaru Morisada ◽  
Hirokuni Kaku ◽  
Taka-aki Onodera ◽  
Ryu Kurokawa
Keyword(s):  
Endothelial Cell ◽  
Arterial Wall ◽  
Cell Layer ◽  
Low Calcium ◽  
Endothelial Cell Layer

Abstract 11809: Trans-Endothelial Electrical Resistance to Assess Cell Layer Integrity in Coronary Artery Endothelial Cells After Hypoxia/Reoxygenation Injury

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Matthew J Hampton ◽  
Insha H Maknojia ◽  
zhu li ◽  
Matthew B Barajas ◽  
Matthias L Riess
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Coronary Artery ◽  
Electrical Resistance ◽  
Cell Layer ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Membrane Integrity ◽  
Cardiac Cells

Introduction: Cardiovascular disease remains one of the leading causes of complications and death worldwide. Therefore, accurate and reliable methods of mimicking ischemia/reperfusion (IR) injury in cardiac cells in vivo are crucial when testing drugs/substances for prevention and treatment. Coronary artery endothelial cells play a critical role in not only supplying blood to myocardial cells but protecting them from insult as well. However, the endothelial layer can be compromised by ischemic injury, heightening damage to the heart during reperfusion. Hypothesis: Varied ischemic insult of mouse coronary artery endothelial cells (MCAECs) affects cell layer integrity as measured by Trans-Endothelial Electrical Resistance (TEER). Methods: MCAECs were cultured on Grenier Bio-One ThinCert™-cell culture inserts for 72 hrs to allow for adequate confluency. Cells were then subjected to either continued normoxic conditions or hypoxia for 3, 6, 12, or 24 hrs, with a 2-hr reperfusion period immediately following. TEER was used to measure the integrity of the endothelial cell layer on the insert. Results: Our data showed a significant decrease in TEER between control and hypoxic groups after 6 hrs (p = 0.0400), 12 hrs (p = 0.0179) and 24 hrs (p = 0.0103), but not after 3 hrs (p = 0.4453) of hypoxia. Conclusion: This indicates that titrating the hypoxia time to a sufficient duration is necessary to achieve an adequate H/R injury which can then be used for potential cardioprotective agents and/or strategies to be tested. Furthermore, TEER is a reliable and reproducible method to assess the role of endothelial cell membrane integrity in cardioprotection.

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