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PubMed1983

Membrane traffic in Dictyostelium discoideum: plasma membrane glycoconjugates internalized and recycled during fluid phase pinocytosis enter the Golgi complex.

Plasma membrane glycoconjugates, enzymatically labelled with [3H]galactose, were used as an autoradiographic membrane marker for a morphometric analysis of membrane traffic during fluid phase pinocytosis in the amoeba, Dictyostelium discoideum. The fraction of grains associated with the plasma membrane decreased exponentially from 99% for cells fixed directly after labelling on the cell surface, to a steady-state value of 45% after about 1 h of pinocytotic activity. The complementary fraction of grains was observed on vacuolar membranes. Only after a lag of about 20 min, a small but significant fraction (3%) of the total grains, was found in the region of the Golgi membranes. During two subsequent doublings of cell number, over a period of 24 h, label was lost into the medium at a constant rate of 1% per h. The cell bound label remained fully membrane bound over the entire period. The beta(1-4) linkage was not noticeably modified, as judged by its susceptibility to hydrolytic release by beta-galactosidase. An analysis by SDS-polyacrylamide gel electrophoresis (SDS-PAGE) showed an identical labelling pattern for total membrane fractions when prepared directly after labelling or after 24 h of membrane flow.

Biological Transport, Active↗

PubMed1982

Coated pits and pinocytosis of cationized ferritin in human skin fibroblasts.

Pinocytosis was studied in cultured human skin fibroblasts in order to obtain more information about uptake in these cells of non-specific ligands with different net surface charge. The fibroblasts were obtained from a normal person and a patient homozygous for familial hypercholesterolemia. No ultrastructural differences were observed between the two cell types. The ratio between coated and smooth pits at the cell surface was about 1:6. Freeze-fracture revealed that whereas smooth pits were devoid of intramembrane particles, the coated pits occupying 1-5% of the total cell surface area showed numerous intramembrane particles. Cationized ferritin (pI = 8.5) bound to the cell surface and to coated pits of both types of fibroblasts at 4 degrees C. Either type internalized CF at 37 degrees C. Vacuoles (lysosomal elements) containing CF were seen already after 5 min at 37 degrees C, but were much numerous after 30 min of incubation at 37 degrees C, and appeared with the same frequency in both cell types. Smooth (uncoated) pits at the cell surface remained unlabeled. In contrast to CF, native ferritin (pI = 4.6) was internalized to a very limited extent in both cell types, even after 3.5 h of incubation at 37 degrees C. These results indicate that both normal and FH fibroblasts internalize CF exclusively by coated pits, and adsorptive uptake mechanism that apparently is nonspecific but clearly cation-selective.

Adolescent↗

PubMed1981

[Electron microscopic study of horseradish peroxidase pinocytosis by white rat peritoneal macrophages in vivo].

Pinocytic activity of rat peritoneal macrophages has been studied morphometrically at the ultrastructural level, 1.5-50 minutes following the intraperitoneal administration of horseradish peroxidase at varying concentrations. Internalization of the tracer was carried out by relatively large vacuoles and coated microvesicles. A probable mechanism underlying the two structurally distinct kinds of pinocytosis by macrophages is discussed.

Animals↗

PubMed1993

[Ultrastructural study of transepithelial pinocytosis induced by endotoxin in the distal section of the nephron].

In initial and intermediate periods of endotoxin shock in rats and dogs significant micropinocytosis in the epithelial cells of distal tubules and collecting ducts are observed. On the stage of late endotoxemia in rats transepithelial pinocytosis disappears. Existence of correlative connections between ultrastructural changes in neurosecretory system and epithelial cells responsible for facultative reabsorption in different periods of experimental endotoxemia have been shown.

Animals↗

PubMed1993

Modulation of actin microfilament dynamics and fluid phase pinocytosis by phosphorylation of heat shock protein 27.

We recently reported that overexpression of heat shock protein 27 (HSP27) in rodent fibroblasts increases the stability of stress fibers during hyperthermia and partially prevents actin depolymerization during exposure to cytochalasin D (Lavoie, J.N., Gingras-Breton, G., Tanguay, R. M., and Landry, J. (1993) J. Biol. Chem. 268, 3420-3429). Because HSP27 is a ubiquitous target of phosphorylation upon cell stimulation with a variety of growth factors and agents that affect cellular differentiation, we examined the role of HSP27 phosphorylation in regulating actin filament dynamics. Here we show that HSP27 is enriched at the leading edge of polarized fibroblasts. HSP27 is localized in lamellipodia and membrane ruffles where most actin polymerization occurs. We developed Chinese hamster cell lines that constitutively overexpressed either human HSP27 or a nonphosphorylatable mutant form of the protein. Overexpression of HSP27 caused an increased concentration of filamentous actin (F-actin) at the cell cortex and elevated pinocytotic activity. In contrast, overexpression of the non-phosphorylatable mutant form of HSP27 reduced cortical F-actin concentration and decreased pinocytosis activity relative to control cells. Mitogenic stimulation of fibroblasts resulted in a rapid polymerization of submembranous actin filaments. HSP27 enhanced growth factor-induced F-actin accumulation, whereas mutant HSP27 exerted a dominant negative effect and inhibited this response to growth factors. Thus, HSP27 is a component of a signal transduction pathway that can regulate microfilament dynamics.

Actins↗

PubMed1993

A quantitative assessment of non specific pinocytosis by human endothelial cells surviving in vitro.

Human umbilical vein endothelial cells have been assayed in vitro, 24 hrs. after plating, for non specific pinocytic activity. The culture conditions were designed to minimize the exogenous stimulations of pinocytosis, such as those possibly coming from mitotic induction and chemical and contact-dependent signaling. Two different markers were used: Lucifer Yellow CH (LY), and three different preparations of horseradish peroxidase, a multiple form (type II) composed of five different isoenzymes, and two purified acidic (type VIII) and basic (type IX) isoenzymes. The uptake of LY appears to depend on both fluid-phase incorporation and non specific adsorption to the cell surface, and it shows a linear monophasic dependence on time and a linear diphasic dependence on concentration. This probe is actively chased from the cells to an extent proportional to the amount incorporated. Therefore, the endocytic index obtained from the LY incorporation data is not a reliable estimate of extracellular fluid incorporation. The three different forms of HRP share an incorporation pattern linearly dependent on both time and concentration, consistent with the classical interpretation of a simple fluid-phase mechanism of intracellular uptake; however, the rates of uptake and chase activity of the pure isoenzymes are clearly different from that of the multiple form. The observed differences are related to possible local variations in the physicochemical properties of the cell surface, which may restrict the cell surface area suitable for fluid-phase uptake of differently charged macromolecular probes.

Cells, Cultured↗

PubMed1977

Effect of glucagon on pinocytosis by the yolk sac of the rat.

The uptake of macromolecular markers by fluid pinocytosis in the rat yolk sac was inhibited by glucagon, with half-maximal effect at a hormone concentration of approximately 3 X 10(-8) M. Glucagon had no effect on the cellular distribution of the marker subsequent to its uptake. Rates of uptake promptly returned to normal when the yolk sacs were transferred from a glucagon-containing to a glucagon-free medium. Epinephrine also inhibited, but only at much higher concentrations. The effect of the latter was augmented by theophylline. Insulin (10(-6) M) had no effect when added alone or with an inhibitory level of glucagon (10(-7) M). The presumption that the hormone effect was mediated by cyclic AMP was supported by the findings that the cellular levels of cyclic AMP were elevated in the presence of glucagon and that dibutyryl cyclic AMP could replace glucagon as an effective inhibitor. The conclusion that the hormone effect was on uptake rather than on subsequent regurgitation was based on the linearity of accumulation in both the presence and absence of glucagon and the inability of glucagon to stimulate loss of invertase from preloaded cells. Colchicine and vinblastine also inhibited uptake. This finding and those of others which are discussed suggest the possibility that effects of cyclic nucleotides on certain cell functions may involve their regulation of microtubular status.

Animals↗

PubMed1997

Differences between fluid-phase endocytosis (pinocytosis) and receptor-mediated endocytosis in isolated rat hepatocytes.

To characterize possible differences between the fluid-phase endocytosis (pinocytosis) of bovine serum albumin and the receptor-mediated endocytosis of asialo-orosomucoid (AOM) in isolated rat hepatocytes, both probes were conjugated to radioiodinated tyramine-cellobiose, [125I]TC. The use of these conjugates made it possible to measure the uptake and intracellular distribution of the intact proteins as well as of their acid-soluble, membrane-impermeant degradation products. [125I]TC-albumin was taken up at a very low rate (0.5%/h) compared to [125I]TC-AOM (45%/h), suggesting that neither membrane adsorption nor membrane permeation compromised its suitability as a fluid-phase marker. Sucrose gradient analysis indicated that both probes sequentially entered light endosomes (1.11 g/ml), dense endosomes (1.14 g/ml) and lysosomes (1.18 g/ml), but [125I]TC-albumin traversed the endocytic compartments more rapidly than [125I]TC-AOM, and was partially degraded intralysosomally already after 15 min. The microtubule inhibitor, vinblastine, had a stronger inhibitory effect on the uptake and degradation of [125I]TC-AOM (80% and 95%, respectively) than on the uptake and degradation of [125I]TC-albumin (50% and 70%, respectively). In the presence of vinblastine, [125I]TC-AOM was retained both in light and dense endosomes, whereas [125I]TC-albumin was retained in dense endosomes only, suggesting that the early steps of fluid-phase endocytosis were less critically dependent on microtubular function than the early steps of receptor-mediated endocytosis. A perturbant of vacuolar pH, propylamine, inhibited the degradation of both probes strongly (75-100%), as would be expected from its lysosomotropic effect. Propylamine also inhibited endocytic uptake, with a stronger effect on [125I]TC-AOM uptake (95% inhibition) than on [125I]TC-albumin uptake (60% inhibition), probably reflecting a reduction in endosomal acidity, reduced receptor-ligand dissociation and diminished recycling of free asialoglycoprotein receptors to the cell surface in addition to a general trapping of membrane in swollen vacuoles. A protein phosphatase inhibitor, okadaic acid, strongly (80-100%) inhibited the uptake and degradation of both [125I]TC-albumin and [125I]TC-AOM. An inhibitor of lysosomal proteinases, leupeptin, strongly suppressed the degradation of both probes and moderately reduced the uptake of [125I]TC-AOM, whereas the uptake of [125I]TC-albumin was unaffected. In contrast, an inhibitor of autophagic sequestration, 3-methyladenine, reduced both the uptake and degradation of [125I]TC-albumin markedly (55% and 75%, respectively), with considerably less effect on [125I]TC-AOM (25% and 35%, respectively). As autophagy-inhibitory amino acid mixture did not share these effects, suggesting that 3-methyladenine may suppress endocytic fluid-phase uptake by an autophagy-independent mechanism. Fluid-phase and receptor-mediated endocytosis in hepatocytes thus appear to differ with respect to uptake mechanisms as well as in the kinetics by which endocytosed material traverses the endocytic-lysosomal pathway.

Animals↗

PubMed1964