Plasma Membrane Fluidity and Surface Motility of Mouse C-1300 Neuroblastoma Cells

1973 ◽  
Vol 13 (2) ◽  
pp. 415-420
Author(s):  
P. M. COMOGLIO ◽  
G. FILOGAMO

Under suitable conditions, topographical redistribution of plasma membrane molecules with oligosaccharide residues specifically bound by Concanavalin-A can be induced on neuroblastoma C-1300 cells. This shows that transformed nerve cell membrane is fluid at 37 °C and provides further support for the suggestion that such fluidity may be a common property of all animal cells. As previously reported for mesenchymal cells (lymphocytes and fibroblasts), clustering of Concanavalin-A binding sites on the cell surface is dependent on temperature and on reagent concentration. The formation of larger aggregates, known as patches or polar caps, requires metabolic energy provided by the cell. In fibroblasts caps are formed in as little as 15-30 min. C-1300 neuroblastoma cells, however, need several hours of incubation before patches or, more rarely, single caps appear. The mechanism of formation of patches and caps is discussed with reference to cell membrane fluidity and the possibility that there exists a membrane motility characteristic of each cell type.

1995 ◽  
Vol 23 (4) ◽  
pp. 254-263 ◽  
Author(s):  
M Marutaka ◽  
H Iwagaki ◽  
K Mizukawa ◽  
N Tanaka ◽  
K Orita

The time-course of changes in the plasma-membrane lipid bilayer induced by tumour necrosis factor-α (TNF) were investigated in cultured cells using spin-label electron-spin-resonance techniques. Treatment of K 562 cells, a human chronic myelocytic leukaemia cell line, in suspension culture with TNF for up to 6 h caused an initial increase in cell-membrane fluidity, which returned to the control level after 12 h of treatment. After 24 h of treatment, the cell-membrane fluidity had decreased and this decrease was maintained after 48 h of treatment. In Daudi cells, a human malignant lymphoma cell line, TNF, did not induce any changes in cell-membrane fluidity, indicating that the effect of TNF on membrane structure is cell-specific. The early and transient change in membrane fluidity in K 562 cells is probably related to signal generation, while the later, persistent change may reflect the phenotype of TNF-treated cells, in particular, changes in the plasma membrane-cytoplasmic complex. Histochemical electron microscopic studies indicated that the membrane fluidity changes induced by TNF have an ultrastructural correlate.


1989 ◽  
Vol 4 (3) ◽  
pp. 221-227 ◽  
Author(s):  
ANTONIO BENEDETTI ◽  
GIANNA FERRETTI ◽  
GIOVANNA CURATOLA ◽  
EUGENIO BRUNELLI ◽  
ANNE MARIE JÉZÉQUEL ◽  
...  

1994 ◽  
Vol 3 (7) ◽  
pp. S21-S24 ◽  
Author(s):  
A. Kantar ◽  
N. Oggiano ◽  
P. L. Giorgi ◽  
G. V. Coppa ◽  
R. Gabbianelli ◽  
...  

The effect of nedocromil sodium on the plasma membrane fluidity of polymorphonuclear leukocytes (PMNs) was investigated by measuring steady-state fluorescence anisotropy of 1-[4-trimethylammonium-phenyl]-6-phenyl- 1,3,5-hexatriene (TMA-DPH) incorporated in the membrane. Our results show that nedocromil sodium 300 μM significantly decreased membrane fluidity of PMNs. The decrease in membrane fluidity of PMNs induced by fMLP was abolished in the presence of nedocromil sodium. These data suggest that nedocromil sodium interferes with the plasma membranes of PMNs and modulates their activities.


1979 ◽  
Vol 64 (2) ◽  
pp. 315-326 ◽  
Author(s):  
Thomas B. Eckstein ◽  
William R. Randall ◽  
Mark G. McNamee

1988 ◽  
Vol 254 (6) ◽  
pp. C781-C787 ◽  
Author(s):  
N. P. Sheridan ◽  
E. R. Block

Plasma membrane vesicles were prepared from porcine pulmonary artery endothelial cells by a dextran-polyethylene glycol two-phase system. Specific carrier-mediated transport of 5-hydroxytryptamine (5-HT) into the vesicles was examined. Transport required a Na+ gradient (out greater than in) across the membrane, and accumulated 5-HT rapidly effluxed out of the vesicles when the ionophore gramicidin was added. Transport was inhibited by the antidepressant imipramine. 5-HT transport into plasma membrane vesicles appeared saturable and exhibited Michaelis-Menten kinetics (Km 7.4 microM, maximal velocity 217 pmol.min-1.mg membrane protein-1). A 24-h exposure to 95% O2 at 1 atmosphere absolute resulted in a 21% decrease (P less than 0.05) in specific 5-HT transport by plasma membrane vesicles. Hyperoxia also caused a significant (P less than 0.01) decrease in plasma membrane fluidity, as measured with the fluorescence probe 1,6-diphenyl-1,3,5-hexatriene. These results indicate that pulmonary artery endothelial cell plasma membrane vesicles provide a good model for studying 5-HT transport activity in vitro. Hyperoxia affects plasma membrane fluidity and 5-HT transport in pulmonary artery endothelial cells, suggesting a possible cause-and-effect relationship between the two.


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