Neutrophil-assisted DNA synthesis by human lymphocytes in response to mevalonic acid; enhancement by cytochalasin B

1983 ◽  
Vol 81 (2) ◽  
pp. 357-372
Author(s):  
Richard A. Larson ◽  
Leo I. Gordon ◽  
Stanley Yachnin
1984 ◽  
Vol 66 (1) ◽  
pp. 155-166
Author(s):  
K.G. Sundqvist ◽  
L. Wanger ◽  
W. Ensgstom

Unfractionated or T-cell-enriched human lymphocytes can be stimulated to undergo DNA synthesis and mitosis by the addition of polyclonal cell activators such as the plant lectins phytohaemagglutinin and concanavalin A (ConA). Under conventional culture conditions stimulated cells cease proliferating only a few days after the first cells have initiated DNA synthesis. Cytochalasin B (CB), which is non-mitogenic per se, causes a prolongation of the period during which ConA stimulates DNA synthesis from normally 3–5 days to more than 3 weeks. The CB-induced prolongation of cell proliferation is clearly stage-specific in the sense that the CB effects are exerted after an initial period of 24 h and do not come into effect until 48 h after onset of ConA stimulation. In contrast, CB exerts a slight suppressive action on DNA synthesis between 24 h (when activated cells initiate DNA synthesis) and 48 h after onset of stimulation. These two separate effects of CB, i.e. augmentation of lymphocyte stimulation 48 h after stimulation, and suppression of stimulation before this point of time, are relatively independent of the concentration of CB.


2006 ◽  
Vol 24 (3) ◽  
pp. 273-281 ◽  
Author(s):  
O. RINGDÉN ◽  
T. PAULIN ◽  
V. A. SUNDQVIST ◽  
B. WAHREN ◽  
P. PIHLSTEDT

1998 ◽  
Vol 56 (9) ◽  
pp. 1175-1179 ◽  
Author(s):  
Mária Sasvári-Székely ◽  
Tatjana Spasokoukotskaja ◽  
Melinda Szóke ◽  
Zsolt Csapó ◽  
Ágnes Turi ◽  
...  

1985 ◽  
Vol 78 (1) ◽  
pp. 87-96
Author(s):  
I. Hickey ◽  
C. McConville ◽  
M. McMenamin ◽  
R. Neill

Cytochalasin B (CB) prevents cytokinesis in animal cells. In normal cells nuclear division and DNA synthesis are also blocked and the cells, held in the G1 phase of the cell cycle, remain either mononucleate or binucleate. In transformed cell lines DNA synthesis and nuclear division continue and the cells become multinucleate. We have examined the response to CB in two sets of somatic cell hybrids made between cells that display multinucleation after CB treatment and cells that do not. In a cross between transformed mouse LMTK cells and normal rat embryo lung cells, very little multinucleation was observed after treatment with CB for 7 days. The ability of the LMTK cells to form clones in soft agar was also significantly reduced in these hybrids. Segregant sub-clones that re-expressed both of these transformation phenotypes were isolated. These had reduced chromosome numbers. A second cross was made between two variants of the BHK cell line, one of which displayed a high level of multinucleation in CB while the other did not. Again the hybrids showed a response similar to that of the non-multinucleating parent. From the results obtained with these two hybrids we conclude that the multinucleation induced in transformed cells by CB behaves as a recessive character in crosses with normal cells.


1987 ◽  
Vol 148 (1) ◽  
pp. 435-442 ◽  
Author(s):  
Alain Pompidou ◽  
Marisol Corral ◽  
Paule Michel ◽  
Nicole Defer ◽  
Jacques Kruh ◽  
...  

Blood ◽  
1981 ◽  
Vol 57 (1) ◽  
pp. 164-169 ◽  
Author(s):  
PC Hoffman ◽  
CM Richman ◽  
RC Hsu ◽  
J Chung ◽  
AM Scanu ◽  
...  

Abstract Oxygenated sterol compounds are potent inhibitors of sterol and DNA synthesis in mammalian cells. We studied the effects of oxygenated sterols on human marrow granulocytic progenitor cells in vitro (CFU-C). 25-Hydroxycholesterol was found to be a potent inhibitor of sterol synthesis in marrow mononuclear cells, with 50% inhibition occurring at approximately 10(-7) M. This compound, as well as 6-ketocholestanol, 7- ketocholesterol, and 20 alpha-hydroxycholesterol, also demonstrated marked inhibition of CFU-C proliferation. The latter effect, which was not a result of direct cytoxicity of the compounds, was reversible by cholesterol, but not by mevalonic acid. We conclude that inhibition of sterol synthesis by oxygenated sterol compounds may be insufficient to explain their suppression of CFU-C proliferation.


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