Surface morphology and agglutination of lectin-treated human lymphocytes and lymphoblasts

1976 ◽  
Vol 21 (3) ◽  
pp. 563-578
Author(s):  
J.H. Temmink ◽  
J.G. Collard ◽  
J. Roosien ◽  
J.F. Van den Bosch
Keyword(s):  
Cell Surface ◽  
Surface Morphology ◽  
Human Lymphocytes ◽  
Cell Type ◽  
A Cell ◽  
Human Peripheral Lymphocytes ◽  
Normal Human ◽  
Altered Cell ◽  
Induced Changes ◽  
Cell Surface Morphology

Two human lymphoblasts (Raji and EB3) and normal human peripheral lymphocytes were exposed to different concentrations of Concanavalin A and wheat germ agglutinin. The lectin-induced agglutination was determined and correlated with lectin-induced changes in the surface morphology of these cells as studied in a scanning electron microscope. Whenever the lectin induced high agglutinability in a cell type, it also invariably had a smoothing effect on the cell surface. In contrast, when cells did not agglutinate well with a certain lectin, their cell surface remained essentially rough (villous) after addition of the lectin. The correlation found between increased agglutinability and altered cell surface morphology upon treatment with certain lectins suggests that both phenomena result from one and the same process. Additional evidence for this postulate is presented.

Human lymphocytes: similarity of B and T cell surface morphology

Science ◽  
1975 ◽  
Vol 188 (4189) ◽  
pp. 732-734 ◽  
Author(s):  
E. Alexander ◽  
B Wetzel
Keyword(s):  
T Cell ◽  
Cell Surface ◽  
Surface Morphology ◽  
Human Lymphocytes ◽  
Cell Surface Morphology

scholarly journals Differential inhibition of nerve growth factor and epidermal growth factor effects on the PC12 pheochromocytoma line.

1984 ◽  
Vol 98 (2) ◽  
pp. 417-426 ◽  
Author(s):  
P J Seeley ◽  
A Rukenstein ◽  
J L Connolly ◽  
L A Greene
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Surface ◽  
Surface Morphology ◽  
Neurite Outgrowth ◽  
Decarboxylase Activity ◽  
Differential Inhibition ◽  
Epidermal Growth ◽  
Cell Surface Morphology

Tests have been made of the action of the methyltransferase inhibitors 5'-S-methyl adenosine, 5'-S-(2-methyl-propyl)-adenosine, and 3-deaza-adenosine +/- L-homocysteine thiolactone, on nerve growth factor (NGF)-dependent events in the rat pheochromocytoma line PC12. Each of these agents inhibited NGF-dependent neurite outgrowth at concentrations of the order of millimolar. Slow initiation of neurite outgrowth over several days and more rapid regeneration of neurites (congruent to 1 d) were blocked, as was the priming mechanism necessary for genesis of neurites. The inhibitions were reversible in that PC12 cells maintained for several days in the presence of inhibitors grew neurites normally after washout of these agents. Other NGF-dependent responses of the PC12 line (i.e., induction of ornithine decarboxylase activity [over 4 h], enhancement of tyrosine hydroxylase phosphorylation [over 1 h], and rapid changes in cell surface morphology [30 s onward]) were inhibited by each of the agents. In contrast, corresponding epidermal growth factor-dependent responses in ornithine decarboxylase activity, phosphorylation, and cell surface morphology were not blocked, but instead either unaffected or enhanced, by the methylation inhibitors. These inhibitors did not act by blockade of binding of NGF to high- or low-affinity cell surface receptors, though they partially inhibited internalization of [125I]NGF. The inhibition of rapidly-induced NGF-dependent events and the differential inhibition of responses to NGF and epidermal growth factor imply that the methyltransferase inhibitors specifically block one of the first steps in the mechanistic pathway for NGF.

PLAG1 enhances the stemness profiles of acinar cells in normal human salivary glands in a cell type-specific manner

2020 ◽  
Vol 62 (1) ◽  
pp. 99-106 ◽  
Author(s):  
Yuriko Goto ◽  
Miho Ibi ◽  
Hirotaka Sato ◽  
Junichi Tanaka ◽  
Rika Yasuhara ◽  
...  
Keyword(s):  
Salivary Glands ◽  
Acinar Cells ◽  
Cell Type ◽  
Specific Manner ◽  
A Cell ◽  
Normal Human ◽  
Cell Type Specific

scholarly journals Mouse Cytomegalovirus Differentially Exploits Cell Surface Glycosaminoglycans in a Cell Type-Dependent and MCK-2-Independent Manner

Viruses ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 31
Author(s):  
Sergio M Pontejo ◽  
Philip M Murphy
Keyword(s):  
Cell Surface ◽  
Target Cells ◽  
Cell Type ◽  
Macrophage Cell ◽  
Virus Binding ◽  
Mouse Cytomegalovirus ◽  
Independent Manner ◽  
A Cell ◽  
Primary Bone ◽  
Primary Bone Marrow

Many viruses initiate interaction with target cells by binding to cell surface glycosaminoglycans (GAGs). Heparan sulfate (HS) appears to be particularly important in fibroblasts, epithelial cells and endothelial cells, where it represents the dominant GAG. How GAGs influence viral infectivity in HS-poor target cells such as macrophages has not been clearly defined. Here, we show that mouse cytomegalovirus (MCMV) targets HS in susceptible fibroblasts and cultured salivary gland acinar cells (SGACs), but not in macrophage cell lines and primary bone marrow-derived macrophages, where chondroitin sulfate was the dominant virus-binding GAG. MCK-2, an MCMV-encoded GAG-binding chemokine that promotes infection of macrophages as part of a gH/gL/MCK-2 entry complex, was dispensable for MCMV attachment to the cell surface and for direct infection of SGACs. Thus, MCMV tropism for target cells is markedly influenced by differential GAG expression, suggesting that the specificity of anti-GAG peptides now under development as HCMV therapeutics may need to be broadened for effective application as anti-viral agents.

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