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At least 253 records · Page 14Linked to original sources
PubMed1984

Reversible pinocytosis of horseradish peroxidase in lymphoid cells.

A detailed study of fluid phase endocytosis of horseradish peroxidase (HRP) in rat lymph node cells (LNC) is presented in this paper. Preliminary experiments have shown that HRP was internalized by non-receptor-mediated endocytosis and interacted minimally or not at all with plasma membrane of LNC, and can then be considered as a true fluid phase marker for these cells. Kinetics of uptake of HRP was found not to be linear with incubation time at 37 degrees C and deviation from linearity can be attributed to constant exocytosis of HRP. The kinetics of exocytosis cannot be described by a single exponential process. Rather, a minimum of two exponentials is required to account for exocytosis. This suggests that at least two intracellular compartments are involved in this process. The first turns over very rapidly with a t 1/2 release of about 3 min and is saturated after 10 min of exposure with HRP. The second, which turns over very slowly, is characterized by a t 1/2 release of about 500 min and accounts for the intracellular accumulation of HRP. Similar biphasic kinetics of exocytosis were observed with unfractionated LNC, with T lymphocyte-enriched LNC and with lymphocytes purified according to their density. This suggests that most, if not all, LNC are able to release HRP and that each cell type is endowed with the two intracellular compartments. Kinetics of uptake of HRP in these two compartments indicated that they are probably filled by two endocytic pathways, at least partially independent. Taken together, these results seem to indicate that a rapid membrane recycling occurs in lymphocytes. Furthermore, the weak base ammonium chloride and the carboxylic ionophore monensin were shown in our study to inhibit fluid phase endocytosis of HRP. The inhibition was time-dependent and required a preincubation of the cells with the drugs to be observed. Our results suggest that a perturbation of the vesicular traffic or a sequestration of membranes involved in HRP uptake is induced by these drugs. Under these conditions the release of cell-associated HRP was also reduced and to the same extent as the inhibition of uptake. Distribution of HRP between the two compartments and the t 1/2 release of HRP from either compartment were not perturbed. Taken together these results seem to indicate that exocytosis is not specifically affected by these drugs. Inhibition of uptake in drug-treated cells could result from a general decrease of membrane recycling or to the formation of smaller pinocytic vesicles with a different surface to volume ratio.

Ammonium Chloride↗
PubMed1984

pH in the endosome. Measurements during pinocytosis and receptor-mediated endocytosis.

By fluorescence spectroscopy, the average pH within endocytic compartments was determined during endocytosis of fluorescein conjugates by macrophages and hepatocytes. In mouse macrophages and hepatocytes fluorescein conjugates taken up either in the fluid phase or by binding to cell surface receptors were rapidly transferred to an acidic compartment (pH 5-5.5). The half-time for this process was generally less than 4 min. The pH within yeast-containing phagosomes was also rapidly reduced to similar levels, following a unique and transient increase. In each case, the acid endosomal compartments involved probably do not contain lysosomal enzymes. When fluorescein conjugates of asialoglycoproteins were internalised by hepatocytes at 20 degrees C, no proteolysis occurred within the acidic endosome until the temperature was raised. Fluorescein conjugates of concanavalin A (conA) and polylysine were relatively more slowly internalised by macrophages. The half-times for uptake, estimated by fluorescence change, were comparable with the turnover time for bulk plasma membrane. The relatively high average pH experienced by these conjugates indicated that a small proportion of these non-specific cell-surface labels was always in contact with the extracellular medium.

Adsorption↗
PubMed1980

Receptor-mediated pinocytosis of mannose glycoconjugates by macrophages: characterization and evidence for receptor recycling.

125I-Mannose--BSA is taken up by alveolar macrophages by receptor-mediated endocytosis. Uptake is macrophage-specific and does not occur in polymorphonuclear leukocytes. Binding (4 degrees C) and uptake (37 degrees C) of 125I--Man--BSA are time- and ligand concentration-dependent [Kuptake = 40 nM; Kd (4 degrees C) = 10 nM]. When adjusted for ligand degradation, ligand uptake is linear with time. Binding saturates at 60 min and requires Ca++. Following binding, ligand remains on the cell surface where it can be released by EGTA and trypsin. Internalization of prebound ligand occurs very rapidly (t 1/2 less than 5 min) when cells are warmed to 37 degrees C. Following internalization of prebound ligand, binding activity is rapidly recovered (t 1/2 less than 5 min). Trypsin treatment (4 degrees C) substantially reduces binding activity (greater than 70% per 30 min). However, binding activity is rapidly recovered in cells treated with trypsin at 4 degrees C by warming to 37 degrees C in the absence of added ligand. Trypsin treatment at 37 degrees C rapidly destroys binding and uptake. On the contrary, 4 degrees C trypsin treatment produces only a modest reduction in subsequent ligand uptake. These results, taken together with the observation that cycloheximide has no effect on ligand uptake, suggest that receptors must be spared from degradation and that reutilization of receptors probably occurs.

Animals↗
PubMed1979

Mechanism of polycation stimulation of pinocytosis.

Synthetic polycations cause a stimulation in the rate of tissue accumulation of colloidal 198Au by the rat visceral yolk sac (at 17.5 days of gestation) and rat peritoneal macrophages cultured in vitro. The mechanism of stimulation has been elucidated in these two cell types by using a dual-substrate technique, and by examining the differential effects of poly(D-lysine) and poly(L-lysine) and of metabolic and cytoskeletal inhibitors. Polycations cause aggregation of colloidal 198Au in the culture medium and increase its affinity for the plasma membrane. In the rat peritoneal macrophage this polycation-colloidal gold complex is pinocytosed, thus enhancing the intracellular accumulation of the radio-labelled substrate. In contrast, the rat visceral yolk sac cannot internalize this complex, and so the substrate accumulates extracellularly. This mechanism of polycation modification affords the opportunity for differential uptake of a substrate into distinct cell types.

Animals↗
PubMed1959

Pinocytosis.

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Cell Biology↗