Quantitative Evaluation of Micro-motion of Vascular Endothelial Cells in Electrical Cell-substrate Impedance Sensing (ECIS) Method Using a Precision Mathematical Model

2006 ◽  
Author(s):  
Noriko Goda ◽  
Yoshitake Yamamoto ◽  
Takao Nakamura ◽  
Toshimasa Kusuhara ◽  
Satoshi Mohri ◽  
...  
Keyword(s):  
Mathematical Model ◽  
Endothelial Cells ◽  
Quantitative Evaluation ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Impedance Sensing ◽  
Cell Substrate ◽  
Micro Motion

scholarly journals EVALUATION OF MICROMOTION OF VASCULAR ENDOTHELIAL CELLS IN ELECTRICAL CELL-SUBSTRATE IMPEDANCE SENSING (ECIS) METHOD USING A MATHEMATICAL MODEL

2005 ◽  
Vol 05 (02) ◽  
pp. 357-368 ◽  
Author(s):  
NORIKO GODA ◽  
NORIYUKI KATAOKA ◽  
JUICHIRO SHIMIZU ◽  
SATOSHI MOHRI ◽  
YOSHITAKE YAMAMOTO ◽  
...  
Keyword(s):  
Mathematical Model ◽  
Endothelial Cells ◽  
Cell Membrane ◽  
Culture Medium ◽  
Cultured Cells ◽  
Vascular Endothelial Cells ◽  
Shielding Effect ◽  
Total Resistance ◽  
Impedance Sensing ◽  
Cell Substrate

We proposed a mathematical model for the microdynamics of cultured cells measured with ECIS (Electrical Cell-substrate Impedance Sensing) system that can separately evaluate cell-to-cell and cell-to-substrate gaps. Our mathematical model is composed of culture medium impedance between cells (Zsol), cell impedance (Zc), and polarization impedance of the electrode (Zp). Zsol consists of the resistance between cells (Rsol) and the capacitance between cells (Csol) of the culture medium. In particular, Rsol is the resistance component related to the cell-to-cell distance (A). Zc consists of capacitance of the cell membrane (Cc) and resistance of the cell membrane (Rc). Zp depends on the cell-to-substrate distance (h) because of the shielding effect of cells to the electrode. The shielding effect is defined as shielding coefficient (Sk). We examined the changes in the impedance of the electrode without or with cells in various conditions. The electrical characteristics of the electrode with or without cells agreed well with those measured in ECIS system. It was found that whether A or h caused the changes in the impedance could be determined based on the changes in the total resistance and reactance (capacitance); A mainly affects the total resistance value, and h mainly affects total capacitance value. Therefore, we can simply estimate the changes in cell-to-cell and cell-to-substrate gaps with measured total resistance and reactance (capacitance). Based on these results, when the cultured endothelial cells (HUVEC) were stimulated with estrogen for 40 hours, it was proved that the cell-to-cell distances decreased, even though the cell-to-electrode distances slightly increased. This result suggests that the barrier function of endothelium is fortified by estrogen.

A mathematical model of plasma membrane electrophysiology and calcium dynamics in vascular endothelial cells

2007 ◽  
Vol 293 (1) ◽  
pp. C277-C293 ◽  
Author(s):  
Haroldo S. Silva ◽  
Adam Kapela ◽  
Nikolaos M. Tsoukias
Keyword(s):  
Mathematical Model ◽  
Endothelial Cells ◽  
Plasma Membrane ◽  
Vascular Tone ◽  
Vascular Endothelial Cells ◽  
Anion Channel ◽  
Ionic Species ◽  
Vascular Endothelial ◽  
Health And Disease ◽  
Vascular Autoregulation

Vascular endothelial cells (ECs) modulate smooth muscle cell (SMC) contractility, assisting in vascular tone regulation. Cytosolic Ca2+ concentration ([Ca2+]i) and membrane potential ( Vm) play important roles in this process by controlling EC-dependent vasoactive signals and intercellular communication. The present mathematical model integrates plasmalemma electrophysiology and Ca2+ dynamics to investigate EC responses to different stimuli and the controversial relationship between [Ca2+]i and Vm. The model contains descriptions for the intracellular balance of major ionic species and the release of Ca2+ from intracellular stores. It also expands previous formulations by including more detailed transmembrane current descriptions. The model reproduces Vm responses to volume-regulated anion channel (VRAC) blockers and extracellular K+ concentration ([K+]o) challenges, predicting 1) that Vm changes upon VRAC blockade are [K+]o dependent and 2) a biphasic response of Vm to increasing [K+]o. Simulations of agonist-induced Ca2+ mobilization replicate experiments under control and Vm hyperpolarization blockade conditions. They show that peak [Ca2+]i is governed by store Ca2+ release while Ca2+ influx (and consequently Vm) impacts more the resting and plateau [Ca2+]i. The Vm sensitivity of rest and plateau [Ca2+]i is dictated by a [Ca2+]i “buffering” system capable of masking the Vm-dependent transmembrane Ca2+ influx. The model predicts plasma membrane Ca2+-ATPase and Ca2+ permeability as main players in this process. The heterogeneous Vm impact on [Ca2+]i may elucidate conflicting reports on how Vm influences EC Ca2+. The present study forms the basis for the development of multicellular EC-SMC models that can assist in understanding vascular autoregulation in health and disease.

The Endothelial Cell and the Factor VIII Bypassing Activity of Prothrombin Complex Concentrate

1988 ◽  
Vol 60 (02) ◽  
pp. 226-229 ◽  
Author(s):  
Jerome M Teitel ◽  
Hong-Yu Ni ◽  
John J Freedman ◽  
M Bernadette Garvey
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Factor Viii ◽  
Prothrombin Complex Concentrate ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Monolayer Cultures ◽  
Coagulant Activity ◽  
Time Courses ◽  
Privileged Site

SummarySome classical hemophiliacs have a paradoxical hemostatic response to prothrombin complex concentrate (PCC). We hypothesized that vascular endothelial cells (EC) may contribute to this “factor VIII bypassing activity”. When PCC were incubated with suspensions or monolayer cultures of EC, they acquired the ability to partially bypass the defect of factor VIII deficient plasma. This factor VIII bypassing activity distributed with EC and not with the supernatant PCC, and was not a general property of intravascular cells. The effect of PCC was even more dramatic on fixed EC monolayers, which became procoagulant after incubation with PCC. The time courses of association and dissociation of the PCC-derived factor VIII bypassing activity of fixed and viable EC monolayers were both rapid. We conclude that EC may provide a privileged site for sequestration of constituents of PCC which express coagulant activity and which bypass the abnormality of factor VIII deficient plasma.

Alterations in Vascular Endothelial Cell-related Plasma Proteins In Thalassaemic Patients and their Correlation with Clinical Symptoms

1995 ◽  
Vol 74 (04) ◽  
pp. 1045-1049 ◽  
Author(s):  
P Butthep ◽  
A Bunyaratvej ◽  
Y Funahara ◽  
H Kitaguchi ◽  
S Fucharoen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Immunosorbent Assay ◽  
Plasma Proteins ◽  
Clinical Symptoms ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Enzyme Linked Immunosorbent Assay ◽  
Vascular Endothelial ◽  
Leg Ulcers

SummaryAn increased level of plasma thrombomodulin (TM) in α- and β- thalassaemia was demonstrated using an enzyme-linked immunosorbent assay (ELISA). Nonsplenectomized patients with β-thalassaemia/ haemoglobin E (BE) had higher levels of TM than splenectomized cases (BE-S). Patients with leg ulcers (BE-LU) were found to have the highest increase in TM level. Appearance of larger platelets in all types of thalassaemic blood was observed indicating an increase in the number of younger platelets. These data indicate that injury of vascular endothelial cells is present in thalassaemic patients.

Actions of Liraglutide on Vascular Endothelial Cells Play a Central Role in the Suppression of Atherosclerosis in Diabetic Mice

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 487-P
Author(s):  
MUNENORI HIROMURA ◽  
YUSAKU MORI ◽  
MASAKAZU KOSHIBU ◽  
HIDEKI KUSHIMA ◽  
KYOKO KOHASHI ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Diabetic Mice

ROCK2 Regulates the Expression of Cell Adhesion Molecules and Cell-to-Cell Adhesion in Vascular Endothelial Cells

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 476-P
Author(s):  
YUSUKE TAKEDA ◽  
KEIICHIRO MATOBA ◽  
DAIJI KAWANAMI ◽  
YOSUKE NAGAI ◽  
TOMOYO AKAMINE ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Cell To Cell Adhesion
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