Homologous liver parenchymal cell-cell adhesion mediated by an endogenous lectin and its receptor |
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Authors: | Saswati?Banerjee Email author" target="_blank">Gopal?Chandra?MajumderEmail author |
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Institution: | (1) University of Pretoria, Hillcrest, Pretoria, South Africa |
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Abstract: | Many studies have implicated cell-surface lectins in heterologous cell-cell adhesion, but little is known about the participation
of lectins in cellular adhesion in homologous cells. Here, we show the development of a cell model for investigating the direct
role of a cell-surface lectin in homologous cell-cell adhesion. Parenchymal cells were isolated from caprine liver using a
perfusion buffer, and dispersed in a chemically defined modified Ringer’s solution. These cells undergo autoagglutination
in the presence of Ca2+. The autoagglutinated cells can be dissociated specifically with D-galactose (50 mM), which also inhibits the liver cell
autoagglutination event. The blood serum protein fetuin has no effect on liver cell autoagglutination, whereas desialylated
fetuin (100 μM), with its terminal D-galactose residue, showed a high affinity for blocking the autoagglutination event. The
data demonstrates the occurrence of a Ca2+-dependent D-galactose-specific lectin and a lectin receptor on the parenchymal cells. Furthermore, it shows that the observed
autoagglutination event is caused by the interaction of the cell-surface lectin with its receptor on the neighbouring homologous
cells. The data supports the view that homologous cell-cell contact in mammalian tissues is triggered by such lectin-receptor
interaction and that the previously reported cell-surface adhesive proteins serve as a secondary force to strengthen cell
adhesion. This cell model could be extremely useful for investigating the direct role of cell-surface lectin and its receptor
in homologous cell adhesion in a variety of tissues under normal and pathological conditions. |
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