The measurement of cell adhesiveness by an absolute method

Development ◽  
1969 ◽  
Vol 22 (3) ◽  
pp. 305-325
Author(s):  
A. S. G. Curtis
Keyword(s):  
Cell Adhesion ◽  
Quantitative Method ◽  
Contact Inhibition ◽  
Measuring Cell ◽  
Absolute Method ◽  
Cell Groups ◽  
Qualitative Test ◽  
Absolute Measurements

The development of a quantitative method for measuring cell adhesion would allow tests to be made of a variety of hypotheses concerning the role of cell adhesiveness in many morphogenetic processes, such as segregation (Steinberg, 1963; Curtis, 1960, 1967), contact inhibition of movement (Abercrombie, 1961), malignancy, etc. Furthermore, the development of a quantitative method giving absolute measurements of cell adhesiveness would be of considerable value in that it would allow critical experiments to be made to test hypotheses about the mechanism of cell adhesion. Basically, two methods exist for the measurement of cellular adhesiveness: (i) a measure of the force or energy required to reseparate two cells or a group of cells from one another or from a non-cellular substrate; (ii) a measure of the forces or energies of interaction involved in bringing two cells or cell groups into adhesion. The first method was introduced as a qualitative test of adhesiveness by Dan (1936).

scholarly journals Emergent structures and dynamics of cell colonies by contact inhibition of locomotion

2016 ◽  
Vol 113 (51) ◽  
pp. 14621-14626 ◽  
Author(s):  
Bart Smeets ◽  
Ricard Alert ◽  
Jiří Pešek ◽  
Ignacio Pagonabarraga ◽  
Herman Ramon ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Cancer Progression ◽  
Broad Spectrum ◽  
Contact Inhibition ◽  
Tissue Morphogenesis ◽  
Cell Clusters ◽  
Dynamic Cell ◽  
Cell Motion ◽  
Cell Extrusion

Cells in tissues can organize into a broad spectrum of structures according to their function. Drastic changes of organization, such as epithelial–mesenchymal transitions or the formation of spheroidal aggregates, are often associated either to tissue morphogenesis or to cancer progression. Here, we study the organization of cell colonies by means of simulations of self-propelled particles with generic cell-like interactions. The interplay between cell softness, cell–cell adhesion, and contact inhibition of locomotion (CIL) yields structures and collective dynamics observed in several existing tissue phenotypes. These include regular distributions of cells, dynamic cell clusters, gel-like networks, collectively migrating monolayers, and 3D aggregates. We give analytical predictions for transitions between noncohesive, cohesive, and 3D cell arrangements. We explicitly show how CIL yields an effective repulsion that promotes cell dispersal, thereby hindering the formation of cohesive tissues. Yet, in continuous monolayers, CIL leads to collective cell motion, ensures tensile intercellular stresses, and opposes cell extrusion. Thus, our work highlights the prominent role of CIL in determining the emergent structures and dynamics of cell colonies.

Platelet and Shear Rate Promote Tumor Cell Adhesion to Human Endothelial Extracellular Matrix - Absence of a Role for Platelet Cyclooxygenase

1989 ◽  
Vol 61 (03) ◽  
pp. 485-489 ◽  
Author(s):  
Eva Bastida ◽  
Lourdes Almirall ◽  
Antonio Ordinas
Keyword(s):  
Cell Adhesion ◽  
Shear Rate ◽  
Tumor Cell ◽  
Umbilical Vein ◽  
Blood Platelets ◽  
Flow Conditions ◽  
Tumor Cell Adhesion ◽  
Rate Dependent ◽  
Static Conditions

SummaryBlood platelets are thought to be involved in certain aspects of malignant dissemination. To study the role of platelets in tumor cell adherence to vascular endothelium we performed studies under static and flow conditions, measuring tumor cell adhesion in the absence or presence of platelets. We used highly metastatic human adenocarcinoma cells of the lung, cultured human umbilical vein endothelial cells (ECs) and extracellular matrices (ECM) prepared from confluent EC monolayers. Our results indicated that under static conditions platelets do not significantly increase tumor cell adhesion to either intact ECs or to exposed ECM. Conversely, the studies performed under flow conditions using the flat chamber perfusion system indicated that the presence of 2 × 105 pl/μl in the perfusate significantly increased the number of tumor cells adhered to ECM, and that this effect was shear rate dependent. The maximal values of tumor cell adhesion were obtained, in presence of platelets, at a shear rate of 1,300 sec-1. Furthermore, our results with ASA-treated platelets suggest that the role of platelets in enhancing tumor cell adhesion to ECM is independent of the activation of the platelet cyclooxygenase pathway.

ANDROST-5-ENE-3β,17β-DIOL IN OVARY OF POST-MENOPAUSAL HYPEROESTROGENIC WOMEN

1968 ◽  
Vol 58 (3) ◽  
pp. 364-376 ◽  
Author(s):  
S. Pesonen ◽  
M. Ikonen ◽  
B-J. Procopé ◽  
A. Saure
Keyword(s):  
Ovarian Tissue ◽  
Cortical Layer ◽  
Vaginal Smears ◽  
Incubation Experiments ◽  
Cell Groups ◽  
Post Menopause ◽  
Reducing Activity ◽  
Post Menopausal ◽  
One Year

ABSTRACT The ovaries of ten patients, at least one year after the post-menopause, were incubated with two Δ5-C19-steroids and also studied histochemically. All these patients had post-menopausal uterine bleeding and increased oestrogen excretion of the urine. The urinary estimations of gonadotrophins, 17-KS, 17-OHCS and pregnanediol were carried out on all patients. Vaginal smears were read according to Papanicolaou, and the endometrium and ovaries were studied histologically. The incubation experiments indicate the presence of Δ5-3β-hydroxysteroid-dehydrogenase. When androst-5-ene-3β,17β-diol was used as precursor the formation of testosterone occurred without any concomitant production of DHA and/or androstenedione. This seems to indicate the possible role of the Δ5-pathway in the formation of testosterone by post-menopausal ovarian tissue. The histochemical reactions indicated a reducing activity on NADH, lactate and glucose-6-phosphate, in certain corpora albicantia, atretic follicles and in diffuse thecoma regions in the cortical layer of the ovary. Steroid-3β-ol-dehydrogenase and β-hydroxybutyrate-dehydrogenase were found only at the edges of certain corpora albicantia, in some individual stroma cell groups and in some atretic follicles. Our studies, both biochemical and histochemical, suggest that the observed increase in the urinary oestrogens of the patients studied might in part at least, be of ovarian origin. This opinion is also supported by the postoperative oestrogen values.

Cell adhesion on chiral surface: The role of protein adsorption

2012 ◽  
Vol 90 ◽  
pp. 97-101 ◽  
Author(s):  
Feng Zhou ◽  
Lin Yuan ◽  
Dan Li ◽  
He Huang ◽  
Taolei Sun ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Protein Adsorption ◽  
Chiral Surface

scholarly journals Serine and Threonine Phosphorylation of the Paxillin LIM Domains Regulates Paxillin Focal Adhesion Localization and Cell Adhesion to Fibronectin

1998 ◽  
Vol 9 (7) ◽  
pp. 1803-1816 ◽  
Author(s):  
Michael C. Brown ◽  
Joseph A. Perrotta ◽  
Christopher E. Turner
Keyword(s):  
Cell Adhesion ◽  
Focal Adhesion ◽  
Binding Sites ◽  
Protein Localization ◽  
Model System ◽  
Lim Domain ◽  
Amino Terminal ◽  
Lim Domains ◽  
Inside Out

We have previously shown that the LIM domains of paxillin operate as the focal adhesion (FA)-targeting motif of this protein. In the current study, we have identified the capacity of paxillin LIM2 and LIM3 to serve as binding sites for, and substrates of serine/threonine kinases. The activities of the LIM2- and LIM3-associated kinases were stimulated after adhesion of CHO.K1 cells to fibronectin; consequently, a role for LIM domain phosphorylation in regulating the subcellular localization of paxillin after adhesion to fibronectin was investigated. An avian paxillin-CHO.K1 model system was used to explore the role of paxillin phosphorylation in paxillin localization to FAs. We found that mutations of paxillin that mimicked LIM domain phosphorylation accelerated fibronectin-induced localization of paxillin to focal contacts. Further, blocking phosphorylation of the LIM domains reduced cell adhesion to fibronectin, whereas constitutive LIM domain phosphorylation significantly increased the capacity of cells to adhere to fibronectin. The potentiation of FA targeting and cell adhesion to fibronectin was specific to LIM domain phosphorylation as mutation of the amino-terminal tyrosine and serine residues of paxillin that are phosphorylated in response to fibronectin adhesion had no effect on the rate of FA localization or cell adhesion. This represents the first demonstration of the regulation of protein localization through LIM domain phosphorylation and suggests a novel mechanism of regulating LIM domain function. Additionally, these results provide the first evidence that paxillin contributes to “inside-out” integrin-mediated signal transduction.

P.1.a.012 New insights from cell adhesion molecules in antidepressant action: role of ITGB3 and GAP43 genes

2014 ◽  
Vol 24 ◽  
pp. S160
Author(s):  
C. Fabbri ◽  
C. Crisafulli ◽  
D. Gurwitz ◽  
J. Stingl ◽  
R. Calati ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Antidepressant Action
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