Cell Proliferation High-Content Screening on Adherent Cell Cultures

2019 ◽  
pp. 299-329
Author(s):  
Pau Carrillo-Barberà ◽  
Jose M. Morante-Redolat ◽  
José F. Pertusa
Keyword(s):  
Cell Proliferation ◽  
Cell Cultures ◽  
High Content Screening ◽  
Adherent Cell

Effects of Altering the Electronics of 2-Methoxyestradiol on Cell Proliferation, on Cytotoxicity in Human Cancer Cell Cultures, and on Tubulin Polymerization

2004 ◽  
Vol 47 (21) ◽  
pp. 5126-5139 ◽  
Author(s):  
Allison B. Edsall ◽  
Arasambattu K. Mohanakrishnan ◽  
Donglai Yang ◽  
Philip E. Fanwick ◽  
Ernest Hamel ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cancer Cell ◽  
Cell Cultures ◽  
Human Cancer ◽  
Tubulin Polymerization ◽  
Human Cancer Cell

scholarly journals Cerebellar granule cells contain a membrane mitogen for cultured Schwann cells.

1989 ◽  
Vol 108 (2) ◽  
pp. 607-611 ◽  
Author(s):  
P W Mason ◽  
J W Bigbee ◽  
G H DeVries
Keyword(s):  
Cell Proliferation ◽  
Schwann Cell ◽  
Schwann Cells ◽  
Cell Cultures ◽  
Granule Cell ◽  
Granule Cells ◽  
Cerebellar Granule Cells ◽  
Proteoglycan Synthesis ◽  
Cerebellar Granule ◽  
Mitogenic Signal

Proliferation of Schwann cells is one of the first events that occurs after contact with a growing axon. To further define the distribution and properties of this axonal mitogen, we have (a) cocultured cerebellar granule cells, which lack glial ensheathment in vivo with Schwann cells; and (b) exposed Schwann cell cultures to isolated granule cell membranes. Schwann cells cocultured with granule cells had a 30-fold increase in the labeling index over Schwann cells cultured alone, suggesting that the mitogen is located on the granule cell surface. Inhibition of granule cell proteoglycan synthesis caused a decrease in the granule cells' ability to stimulate Schwann cell proliferation. Membranes isolated from cerebellar granule cells when added to Schwann cell cultures caused a 45-fold stimulation in [3H]thymidine incorporation. The granule cell mitogenic signal was heat and trypsin sensitive and did not require lysosomal processing by Schwann cells to elicit its proliferative effect. The ability of granule cells and their isolated membranes to stimulate Schwann cell proliferation suggests that the mitogenic signal for Schwann cells is a ubiquitous factor present on all axons regardless of their ultimate state of glial ensheathment.

Development and optimization of a metabolomic method for analysis of adherent cell cultures

2010 ◽  
Vol 404 (1) ◽  
pp. 30-39 ◽  
Author(s):  
Anders P.H. Danielsson ◽  
Thomas Moritz ◽  
Hindrik Mulder ◽  
Peter Spégel
Keyword(s):  
Cell Cultures ◽  
Adherent Cell

Effect of mutagen on cultured Schistosoma mansoni

1986 ◽  
Vol 60 (2) ◽  
pp. 135-142 ◽  
Author(s):  
G. C. Coles ◽  
J. Fitzgerald
Keyword(s):  
Schistosoma Mansoni ◽  
Cell Cultures ◽  
Culture Medium ◽  
Adherent Cell ◽  
Adult Males ◽  
Methane Sulphonate ◽  
Insect Tissue Culture ◽  
Cell Layers ◽  
Large Round

AbstractAlthough lightly homogenized three-week-old Schistosoma mansoni incubated in Mistuhashi and Maramorosch insect tissue culture medium or the medium of Weller and Wheeldon produced adherent cell layers, continued growth of these cells did not occur. Non-adherent cells obtained by trypsinization also failed to produce long term cell cultures even after the addition of a range of growth factors. The possibility of producing tumour-like schistosome cells by the use of the mutagen ethyl methane sulphonate was therefore examined. Four-hour exposure of three-week-old schistosomes caused in some worms (a) large fluid filled ‘ballooning’, which also occurred in adult males, (b) enlargement of the gut, (c) increase in numbers of large round cells within the worms and (d) tissus outgrowths. It is suggested that these effects of mutagen offer new approaches to obtaining permanent schistosome cell cultures.

scholarly journals The requirement for adherent cells in the Fc fragment-induced proliferative response of murine spleen cells.

1979 ◽  
Vol 150 (2) ◽  
pp. 256-266 ◽  
Author(s):  
E L Morgan ◽  
W O Weigle
Keyword(s):  
Cell Proliferation ◽  
B Cells ◽  
B Cell ◽  
B Lymphocytes ◽  
Cell Population ◽  
Proliferative Response ◽  
Adherent Cell ◽  
Adherent Cells ◽  
Spleen Cells ◽  
Murine Spleen

The proliferative response of mouse B lymphocytes induced by Fc fragments was found to be dependent upon an adherent cell population. The adherent cell is esterase positive, irradiation resistant, and not susceptible to lysis by anti-thymus serum and complement. The mechanism(s) by which Fc fragments induce B-cell proliferation could be the result of the interaction of Fc with both B cells and adherent cells or with adherent cells which then release factors that trigger the B cells to proliferate. Spleen cells from the C3H/HeJ mouse were shown to be unable to respond to Fc fragments. The addition of adherent cells from either C3H/St or C3H/HeN mice to adherent cell depleted C3H/HeJ cells enabled them to respond to Fc, indicating the defect was in the adherent cell population.

Cell Proliferation/Cell Death Balance in Renal Cell Cultures after Exposure to a Static Magnetic Field

Nephron ◽  
2001 ◽  
Vol 87 (3) ◽  
pp. 269-273 ◽  
Author(s):  
Michele Buemi ◽  
Demetrio Marino ◽  
Giuseppe Di Pasquale ◽  
Fulvio Floccari ◽  
Massimino Senatore ◽  
...  
Keyword(s):  
Magnetic Field ◽  
Cell Proliferation ◽  
Cell Death ◽  
Cell Cultures ◽  
Static Magnetic Field ◽  
Renal Cell

scholarly journals Granulocyte-macrophage colony-stimulating factor is an endogenous regulator of cell proliferation in juvenile chronic myelogenous leukemia

Blood ◽  
1989 ◽  
Vol 74 (7) ◽  
pp. 2360-2367 ◽  
Author(s):  
RJ Gualtieri ◽  
PD Emanuel ◽  
KS Zuckerman ◽  
G Martin ◽  
SC Clark ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factors ◽  
Chronic Myelogenous Leukemia ◽  
Myelogenous Leukemia ◽  
Adherent Cell ◽  
Semisolid Medium ◽  
Spontaneous Growth ◽  
Gm Csf ◽  
Endogenous Regulator ◽  
Cell Densities

Juvenile chronic myelogenous leukemia (JCML) is a rare myeloproliferative disorder of early childhood that is clinically and cytogenically distinct from the well-recognized adult type of chronic myeloid leukemia. Unlike the adult disease, growth of hematopoietic progenitors from peripheral blood (PB) occurs in the absence of exogenous stimulus even at low cell densities. This so-called “spontaneous”growth can be abrogated by adherent cell depletion and appears to depend on production of endogenous growth factors. We studied seven children with JCML to determine the nature of endogenous stimulators. With isolated PB mononuclear cells (PBMNCs) and a 3H- thymidine (3H-TdR) incorporation assay, JCML cells were shown to incorporate high levels of 3H-TdR when cultured in the absence of stimulus even at low cell densities. When neutralizing antisera prepared against each of the four known colony-stimulating factors (CSFs), GM-CSF, G-CSF, M-CSF, and interleukin-3 (IL-3), as well as antisera against interleukin-1 (alpha and beta) and tumor necrosis factor (TNF) were added to these cultures, only the antisera against recombinant human GM-CSF (rhGM-CSF) consistently resulted in significant inhibition of cell proliferation, achieving up to 72% inhibition of 3H-TdR incorporation in one case. Monoclonal antibodies (MoAbs) against rhGM-CSF resulted in a similar and highly significant degree of inhibition. A marked inhibitory effect of rhGM-CSF antiserum on “spontaneous” growth of PB CFU-GM derived colonies in semisolid medium was also demonstrated in four of five patients studied (87% to 90% inhibition). Production of growth factors by highly enriched JCML monocytes was variable. When initially studied in five of the seven patients, the monocytes from three of the patients revealed increased release of IL-1-like activities; two patients had levels similar to those of controls. One patient with normal levels when initially studied was later shown to have markedly increased amounts of IL-1-like activities in a second preparation of monocyte-conditioned medium (MCM). High levels of GM-CSF were detected in the initial MCM from one patient, but this may have indirectly reflected elevated IL-1-like activities present in the MCM. IL-3 and M-CSF levels were either low or undetectable in the patients studied as compared with MCM prepared with normal adult monocytes. These results clearly implicate GM-CSF as the primary endogenous regulator of JCML cell proliferation in culture and suggest that this malignant myeloproliferative disease may in part result from paracrine stimulation of marrow progenitor cells by growth factors/cytokines secreted by the malignant monocytes.

scholarly journals Pleural Fluid Has Pro-Growth Biological Properties Which Enable Cancer Cell Proliferation

2021 ◽  
Vol 11 ◽  
Author(s):  
Rachelle Asciak ◽  
Nikolaos I. Kanellakis ◽  
Xuan Yao ◽  
Megat Abd Hamid ◽  
Rachel M. Mercer ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Pleural Fluid ◽  
Cancer Cell ◽  
Cell Cultures ◽  
Biological Properties ◽  
Cancer Cell Proliferation ◽  
Different Types ◽  
Pleural Metastases ◽  
Similar Growth

ObjectivesPatients with malignant pleural mesothelioma (MPM) or pleural metastases often present with malignant pleural effusion (MPE). This study aimed to analyze the effect of pleural fluid on cancer cells.Materials and MethodsEstablished patient-derived cancer cell cultures derived from MPE (MPM, breast carcinoma, lung adenocarcinoma) were seeded in 100% pleural fluid (exudate MPM MPE, transudate MPE, non-MPE transudate fluid) and proliferation was monitored. In addition, the establishment of new MPM cell cultures, derived from MPE specimens, was attempted by seeding the cells in 100% MPE fluid.ResultsAll established cancer cell cultures proliferated with similar growth rates in the different types of pleural fluid. Primary MPM cell culture success was similar with MPE fluid as with full culture medium.ConclusionsPleural fluid alone is adequate for cancer cell proliferation in vitro, regardless of the source of pleural fluid. These results support the hypothesis that pleural fluid has important pro-growth biological properties, but the mechanisms for this effect are unclear and likely not malignant effusion specific.

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