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The Biochemical Journal Sep 1996The physiological role of the beta-cell insulin receptor is unknown. To evaluate a candidate function, the insulin regulation of fluid-phase pinocytosis was investigated...
The physiological role of the beta-cell insulin receptor is unknown. To evaluate a candidate function, the insulin regulation of fluid-phase pinocytosis was investigated in a clonal insulinoma cell line (beta TC6-F7) and, for comparison, also in Chinese hamster ovary cells transfected with the human insulin receptor (CHO-T cells). In CHO-T cells, the net rate of fluid-phase pinocytosis was rapidly increased 3-4-fold over the basal rate by 100 nM insulin, with half-maximal stimulation at 2 nM insulin, as assayed by cellular uptake of horseradish peroxidase from the medium. Wortmannin, an inhibitor of phosphatidylinositol (PI)-3-kinase, blocked insulin-stimulated pinocytosis with an IC50 of 7.5 nM without affecting the basal rate of pinocytosis. In insulin-secreting beta TC6-F7 cells, the secretagogues glucose and carbachol (at maximally effective concentrations of 15 mM and 0.5 mM respectively) augmented fluid-phase pinocytosis 1.65-fold over the basal rate. Wortmannin also inhibited secretagogue-stimulated pinocytosis in these beta-cells with an IC50 of 7 nM but did not affect the basal rate of pinocytosis measured in the absence of secretagogues. Wortmannin did not influence either basal or secretagogue-induced insulin secretion. Although these beta TC6-F7 cells have cell-surface insulin receptors, adding exogenous insulin or insulin-like growth factor 1 did not affect their rate of fluid-phase pinocytosis, either in the absence or presence of secretagogues. From these observations, we conclude that: (1) in both insulin-secreting beta-cells and in conventional, insulin-responsive CHO-T cells, a common, wortmannin-sensitive reaction, which probably involves PI-3-kinase, regulates fluid-phase pinocytosis; (2) the insulin-receptor signal transduction pathway is dissociated from the regulation of fluid-phase pinocytosis in the insulin-secreting beta-cell line we studied; and (3) the enhancement of fluid-phase pinocytosis associated with secretagogue-induced insulin release in beta TC6-F7 cells is not attributable to autocrine activation of beta-cell surface insulin receptors.
Topics: Androstadienes; Animals; CHO Cells; Carbachol; Clone Cells; Cricetinae; Glucose; Humans; Insulin; Insulin Antagonists; Insulin Secretion; Insulinoma; Islets of Langerhans; Kinetics; Pancreatic Neoplasms; Pinocytosis; Receptor, Insulin; Recombinant Proteins; Transfection; Wortmannin
PubMed: 8809056
DOI: 10.1042/bj3180623 -
Advances in Immunology 1968
Review
Topics: Antigens; Humans; Hypersensitivity, Delayed; Macrophages; Microscopy, Electron; Microscopy, Phase-Contrast; Monocytes; Phagocytosis; Pinocytosis
PubMed: 4883741
DOI: 10.1016/s0065-2776(08)60443-5 -
The Journal of Biophysical and... Sep 1960
Topics: Albumins; Amoeba; Animals; Coloring Agents; Invertebrates; Phagocytosis; Pinocytosis; Proteus
PubMed: 13692419
DOI: 10.1083/jcb.8.1.288 -
Current Opinion in Microbiology Aug 2012Macropinocytosis has emerged as a major endocytic mechanism in the cell entry of animal viruses. The process differs fundamentally from other endocytic mechanisms... (Review)
Review
Macropinocytosis has emerged as a major endocytic mechanism in the cell entry of animal viruses. The process differs fundamentally from other endocytic mechanisms involved in virus internalization. By activating growth factor receptors or other signaling molecules, plasma membrane-bound viruses trigger the activation of a signaling pathway. When amplified, this causes a transient, global change in cell behavior. The consequences of this change include the actin-dependent formation of membrane protrusions, the elevation of non-specific uptake of fluid, and the internalization of membrane together with surface-bound ligands and particles including viruses. Recent studies show that this strategy is used by a variety of enveloped and non-enveloped viruses.
Topics: Biological Transport; Cell Membrane; Humans; Membrane Fusion; Pinocytosis; Receptors, Cell Surface; Signal Transduction; Virus Internalization
PubMed: 22749376
DOI: 10.1016/j.mib.2012.05.016 -
Revue D'hematologie Dec 1959
Topics: Humans; Leukocytes; Pinocytosis
PubMed: 14433788
DOI: No ID Found -
The Journal of Cell Biology Mar 1985Lucifer Yellow CH (LY) is an excellent probe for fluid-phase pinocytosis. It accumulates within the macrophage vacuolar system, is not degraded, and is not toxic at... (Comparative Study)
Comparative Study
Lucifer Yellow CH (LY) is an excellent probe for fluid-phase pinocytosis. It accumulates within the macrophage vacuolar system, is not degraded, and is not toxic at concentrations of 6.0 mg/ml. Its uptake is inhibited at 0 degree C. Thioglycollate-elicited mouse peritoneal macrophages were found to exhibit curvilinear uptake kinetics of LY. Upon addition of LY to the medium, there was a brief period of very rapid cellular accumulation of the dye (1,400 ng of LY/mg protein per h at 1 mg/ml LY). This rate of accumulation most closely approximates the rate of fluid influx by pinocytosis. Within 60 min, the rate of LY accumulation slowed to a steady-state rate of 250 ng/mg protein per h which then continued for up to 18 h. Pulse-chase experiments revealed that the reduced rate of accumulation under steady-state conditions was due to efflux of LY. Only 20% of LY taken into the cells was retained; the remainder was released back into the medium. Efflux has two components, rapid and slow; each can be characterized kinetically as a first-order reaction. The kinetics are similar to those described by Besterman et al. (Besterman, J. M., J. A. Airhart, R. C. Woodworth, and R. B. Low, 1981, J. Cell Biol. 91:716-727) who interpret fluid-phase pinocytosis as involving at least two compartments, one small, rapidly turning over compartment and another apparently larger one which fills and empties slowly. To search for processes that control intracellular fluid traffic, we studied pinocytosis after treatment of macrophages with horseradish peroxidase (HRP) or with the tumor promoter phorbol myristate acetate (PMA). HRP, often used as a marker for fluid-phase pinocytosis, was observed to stimulate the rate of LY accumulation in macrophages. PMA caused an immediate four- to sevenfold increase in the rate of LY accumulation. Both HRP and PMA increased LY accumulation by stimulating influx and reducing the percentage of internalized fluid that is rapidly recycled. A greater proportion of endocytosed fluid passes into the slowly emptying compartment (presumed lysosomes). These experiments demonstrate that because of the considerable efflux by cells, measurement of marker accumulation inaccurately estimates the rate of fluid pinocytosis. Moreover, pinocytic flow of water and solutes through cytoplasm is subject to regulation at points beyond the formation of pinosomes.
Topics: Animals; Exocytosis; Female; Horseradish Peroxidase; Isoquinolines; Macrophages; Mice; Mice, Inbred ICR; Peroxidases; Phorbols; Pinocytosis; Tetradecanoylphorbol Acetate
PubMed: 3972898
DOI: 10.1083/jcb.100.3.851 -
Methods in Molecular Biology (Clifton,... 2008Eukaryotic cells constantly form and internalize plasma membrane vesicles in a process known as endocytosis. Endocytosis serves a variety of housekeeping and specialized... (Review)
Review
Eukaryotic cells constantly form and internalize plasma membrane vesicles in a process known as endocytosis. Endocytosis serves a variety of housekeeping and specialized cellular functions, and it can be mediated by distinct molecular pathways. Among them, internalization via clathrin-coated pits, lipid raft/caveolae-mediated endocytosis and macropinocytosis/phagocytosis are the most extensively characterized. The major endocytic pathways are usually distinguished on the basis of their differential sensitivity to pharmacological/chemical inhibitors, although the possibility of nonspecific effects of such inhibitors is frequently overlooked. This review provides a critical evaluation of the selectivity of the most widely used pharmacological inhibitors of clathrin-mediated, lipid raft/caveolae-mediated endocytosis and macropinocytosis/phagocytosis. The mechanisms of actions of these agents are described with special emphasis on their reported side effects on the alternative internalization modes and the actin cytoskeleton. The most and the least-selective inhibitors of each major endocytic pathway are highlighted.
Topics: Animals; Caveolae; Clathrin-Coated Vesicles; Endocytosis; Humans; Membrane Microdomains; Phagocytosis; Pinocytosis; Signal Transduction
PubMed: 18369934
DOI: 10.1007/978-1-59745-178-9_2 -
Immunology Apr 2006Macropinocytosis is the actin-dependent formation of large vesicles, which allow the internalization of large quantities of fluid-phase solute. In the majority of cells... (Review)
Review
Macropinocytosis is the actin-dependent formation of large vesicles, which allow the internalization of large quantities of fluid-phase solute. In the majority of cells examined, an exogenous stimulus is required to induce the initiation of this endocytic pathway. However, dendritic cells are thought to constitutively macropinocytose large quantities of exogenous solute as part of their sentinel function. In this review we discuss the evidence that dendritic cells macropinocytose exogenous solute and subsequently present antigenic peptides derived from internalized material to T cells. In addition, we put these data into the context of immune surveillance in vivo.
Topics: Antigen Presentation; Biological Transport; Cytoplasmic Vesicles; Dendritic Cells; Endocytosis; Humans; Pinocytosis; Viruses
PubMed: 16556257
DOI: 10.1111/j.1365-2567.2006.02335.x -
Annals of the New York Academy of... 1987
Review
Topics: Animals; Endocytosis; Male; Microscopy, Electron; Phagocytosis; Pinocytosis; Rats; Sertoli Cells
PubMed: 3328532
DOI: 10.1111/j.1749-6632.1987.tb24994.x -
Comptes Rendus Des Travaux Du... 1958
Topics: Amoeba; Animals; Invertebrates; Pinocytosis; Proteus; Salts
PubMed: 13639534
DOI: No ID Found