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PubMed1971

Cholesterol metabolism in the macrophage. II. Alteration of subcellular exchangeable cholesterol compartments and exchange in other cell types.

Macrophage membrane cholesterol is present in two subcellular cholesterol pools, a rapidly exchanging compartment comprising about two-thirds of the total cholesterol, and a slowly exchanging compartment comprising one-third of the total. The morphological identification of the kinetically distinguishable pools proceeded by alteration of each compartment. Trypsin treatment markedly decreased the rate of cholesterol exchange without removing cholesterol from the membrane. Recovery of normal exchange rates took more than 7 hr and required protein synthesis. This suggested that a plasma membrane receptor is involved in positioning of lipoproteins for exchange, and is consistent with the plasma membrane localization of the rapidly exchanging compartment. Extensive pinocytosis by nondegradable dextran, dextran sulfate, or sucrose resulted in the accumulation of many secondary lysosomes, thus increasing the relative proportion of intracellular membranes. The measurable granule membrane area, cholesterol content, phospholipid content, and the relative size of the slowly exchanging cholesterol compartment all increased. The amount of intracellular membrane altered by extensive phagocytosis of latex particles also increased the size of the slowly exchanging cholesterol compartment. This suggested that the slowly exchanging pool of cholesterol represented the intracellular membranes primarily of lysosomal origin. Rabbit alveolar macrophages and thioglycollate-stimulated peritoneal macrophages contain many secondary lysosomes as a result of multiple bouts of in vivo phagocytosis and pinocytosis. In both of these cells the fast and slow pools are equal in size. The increased cholesterol content was attributable to the increase in the relative size of the slowly exchanging compartment. L-cells and melanoma cells also exchange their cholesterol with that of serum lipoproteins. Both cells contain few cholesterol-rich intracellular membranes, and had lower cellular cholesterol contents. In these cells the slowly exchanging pool was a minor contribution to cell cholesterol. Studies with these cells provided further evidence for the lysosomal membrane and plasma membrane localization of the slowly and rapidly exchanging cholesterol compartments.

Animals↗
PubMed1974

Antigenic modulation in vitro. I. Fate of thymus-leukemia (TL) antigen-antibody complexes following modulation of TL antigenicity from the surfaces of mouse leukemia cells and thymocytes.

The modulation or loss of thymus-leukemia (TL) antigenicity from the surfaces of mouse RADA1 leukemia cells and normal thymocytes during incubation with TL antibody in vitro at 37 degrees C was investigated by cytotoxicity, immunofluorescence, and immunoelectron microscopy. The fate of bivalent and monovalent antibody during modulation was visualized by fluorescence microscopy. Considerable antibody remained bound to the cell surface after modulation, bivalent antibody being displaced topographically into "patches" and "caps" while monovalent antibody was only slightly aggregated on the cell surface. Some antibody was internalized, presumably by pinocytosis, and was sequestered into the Golgi region of the cell. Capping usually occurred over the pole of the cell opposite from the Golgi region, which may explain the lack of extensive pinocytosis of modulating bivalent antibody. Since modulation with monovalent antibody occurs without patch or cap formation, gross topographical redistribution of TL antigen-antibody complexes is not required for modulation, although more subtle displacement of these complexes may be involved. Modulation was demonstrable by cytotoxicity with guinea pig C' but not with absorbed rabbit C', indicating that modulated TL antigens remain bound to the cell surface. A heat-labile factor in TL antiserum and in mouse serum in general is responsible for "blocking" the cytolytic interaction of guinea pig C' with modulated TL antigen-antibody complexes.

Animals↗
PubMed1995

Wortmannin blocks lipid and protein kinase activities associated with PI 3-kinase and inhibits a subset of responses induced by Fc epsilon R1 cross-linking.

We have investigated the effects of wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI 3-kinase), on antigen-mediated signaling in the RBL-2H3 mast cell model. In RBL-2H3 cells, the cross-linking of high affinity IgE receptors (Fc epsilon R1) activates at least two cytoplasmic protein tyrosine kinases, Lyn and Syk, and stimulates secretion, membrane ruffling, spreading, pinocytosis, and the formation of actin plaques implicated in increased cell-substrate adhesion. In addition, Fc epsilon R1 cross-linking activates PI 3-kinase. It was previously shown that wortmannin causes a dose-dependent inhibition of PI 3-kinase activity and also inhibits antigen-stimulated degranulation. We report that the antigen-induced synthesis of inositol(1,4,5)P3 is also markedly inhibited by wortmannin. Consistent with evidence in other cell systems implicating phosphatidylinositol(3,4,5)P3 in ruffling, pretreatment of RBL-2H3 cells with wortmannin inhibits membrane ruffling and fluid pinocytosis in response to Fc epsilon R1 cross-linking. However, wortmannin does not inhibit antigen-induced actin polymerization, receptor internalization, or the actin-dependent processes of spreading and adhesion plaque formation that follow antigen stimulation in adherent cells. Wortmannin also fails to inhibit either of the Fc epsilon R1-coupled tyrosine kinases, Lyn or Syk, or the activation of mitogen-activated protein kinase as measured by in vitro kinase assays. Strikingly, there is substantial in vitro serine/threonine kinase activity in immunoprecipitates prepared from Fc epsilon R1-activated cells using antisera to the p85 subunit of PI 3-kinase. This activity is inhibited by pretreatment of the cells with wortmannin or by the direct addition of wortmannin to the kinase assay, suggesting that PI 3-kinase itself is capable of acting as a protein kinase. We conclude that Fc epsilon R1 cross-linking activates both lipid and protein kinase activities of PI 3-kinase and that inhibiting these activities with wortmannin results in the selective block of a subset of Fc epsilon R1-mediated signaling responses.

Actins↗
PubMed1986

Suppression of endocytosis in neutrophils by influenza A virus in vitro.

The effect of influenza A virus on the endocytic pathway in polymorphonuclear leukocytes (PMNLs) and the relationship of altered endocytic activity to virus-induced inhibition of other PMNL functions were examined with virus that caused decreased phagosomelysosome fusion and bacterial killing (depressing virus [DV]) and virus that did not (non-DV). Binding of both viruses to PMNL surface receptors was similar, but uptake of DV into PMNLs was decreased compared with that of non-DV. Both viruses were associated with the PMNL plasma membrane and were in endosomes. DV caused less stimulation of pinocytosis than did non-DV. The rate of exocytosis of fluoresceinated-dextran (FL-dextran) from cells stimulated with DV was significantly less than for non-DV. When PMNLs were pretreated with buffer, DV, or non-DV and then exposed to FL-dextran and N-formylmethionylleucylphenylalanine, the pinocytosis of FL-dextran was significantly less in cells pretreated with DV as compared with non-DV or buffer.

Endocytosis↗
PubMed1994

HIV-1 infection induces functional alterations in human liver endothelial cells in primary culture.

OBJECTIVES: Since human liver endothelial cells allow HIV-1 multiplication in vitro, we investigated whether HIV induced functional alterations in these cells in primary culture. DESIGN: Direct evidence of the replication of HIV in endothelial cells is sparse, but clotting abnormalities and thrombi, which suggest the existence of an endothelial dysfunction, have been observed in HIV-infected patients. We therefore studied the storage and release of endothelial-specific factors in primary cultures of liver endothelial cells infected with HIV, as well as their cytoskeleton, pinocytic and phagocytic properties. METHODS: Intracellular storage of von Willebrand's factor (vWF) was determined by immunofluorescence and computer image analysis. Excretion of vWF, protein S and endothelin-1 was measured using an enzyme-linked immunosorbent assay and radioimmunoassay. Cytoskeletal constituents were studied by light microscopy. The pinocytosis of acetylated low-density lipoproteins and the phagocytosis of latex beads were analysed under light and electron microscopy. RESULTS: The synthesis of vWF is markedly decreased in HIV-infected liver endothelial cells, as is the excretion of endothelin-1. In contrast, the excretion of protein S remains unaffected and the cytoskeletal network appears to be unaltered. Pinocytosis and phagocytosis are preserved. CONCLUSIONS: HIV infection triggers non-lethal functional alterations in cultured human liver sinusoidal endothelial cells, with a selective impairment in the storage and/or the excretion of endothelial-specific factors such as vWF. This functional modulation could play a role in the pathophysiology of HIV-induced disease.

Cells, Cultured↗
PubMedDate not supplied

Granulocyte-macrophage colony-stimulating factor, interleukin-2, and interleukin-12 synergize with calcium ionophore to enhance dendritic cell function.

The authors previously showed that monocytes treated with calcium ionophore (CI) acquire characteristics of mature dendritic cells (DC) in part through a calcineurin-dependent pathway. In this study, the authors evaluated the ability of granulocyte-macrophage colony stimulating factor (GM-CSF), interleukin-2 (IL-2), and interleukin-12 (IL-12) alone or in combination with CI to induce DC characteristics in peripheral blood monocytes. Monocytes obtained by leukapheresis and countercurrent centrifugal elutriation were cultured with calcium, cytokines, or both, profiled by flow cytometry, and assessed for antigen uptake and sensitization of autologous CD8+ T cells to antigen. Monocytes treated with the combination of GM-CSF, IL-2, and IL-12 resulted in immunophenotypic and antigen uptake profiles typical of immature DC, including loss of surface CD14 expression, de novo low-level expression of B7.1, negligible CD83 expression, marked enhancement of CD40 and ICAM-1, and high major histocompatibility complex class I and II levels. A high level of antigen uptake by macro-pinocytosis was observed. In contrast, CI treatment significantly up-regulates B7.1, B7.2, CD40, CD54, and CD83 and substantially down-regulates CD14 and macro-pinocytosis, a profile consistent with mature DC. Many CI-induced modulations, but none resulting from cytokine treatment alone, were inhibited by the calcineurin phosphatase inhibitor cyclosporin A. Compared with monocytes treated with CI alone, combined treatment of monocytes with GM-CSF, IL-2, IL-12, and CI augmented B7.1 and CD83 expression and enhanced sensitization of autologous CD8+ T cells to melanoma-antigen-derived peptides. These results suggest that several independent pathways of DC activation can cooperatively enhance the function of monocyte-derived DC.

Antigens, CD↗
PubMed1979

Early and late mechanisms of increased vascular permeability following experimental cerebral infarction.

Cerebral infarction was produced in rats by a combination of transient unilateral common carotid artery occlusion and systemic hypoxia. Horseradish peroxidase (HRP) and Evans blue were given 5 minutes prior to sacrifice to assess the integrity of the blood-brain barrier (BBB) at 1 minute, 30 minutes, and 2 hours following the ischemic insult. There was immediate permeability to HRP in the early (1 minute and 30 minutes) post-ischemic period, whereas, Evans blue was not seen until the late (1.5 to 2 hours) post-ischemic period. Ultrastructural examination showed two routes of barrier permeability to HRP. In the early post-ischemic period, HRP was transported by pinocytosis through endothelial cells in areas of brain containing ischemic neurons. In the late post-ischemic period, HRP diffusely leaked into the brain through the necrotic walls of vessels in areas of infarction. In contrast to previous reports, these results show that the BBB becomes permeable immediately following hypoxia-ischemia. In addition, this study shows that BBB permeability to HRP during cerebral ischemia occurs through two mechanisms: an active, energy-requiring permeability through enhanced pinocytosis within endothelial cells and a passive leakage of protein tracers through necrotic vessel walls.

Animals↗
PubMed1985

ATPase and morphologic changes induced by UVB on Langerhans cells in guinea pigs.

We have devised, in guinea pigs, an improved ATPase technique which enables one to proceed from light to electron microscope study while preserving, on the ultrastructural level, the various membranous structures, in particular the Langerhans cell (LC) granules. Using this method, we have been able to confirm the action of acute, low-dose UVB on the surface enzymatic marker, ATPase. Moreover, this study has shown that the ATPase-negative LC contain abnormal LC granules or, more often, are deficient in LC granules. In a previous work, we have shown that, after epicutaneous application of a hapten, one successively observes an extensive adsorptive pinocytosis process, the disappearance of the membranous ATPase system, and the appearance of LC granules in the cytoplasm. Therefore we may suppose that, after UVB irradiation, the disappearance of the ATPase system and/or the possible alteration of the adsorptive pinocytosis process interrupts or alters the formation of LC granules. These successive events might play a vital role in the formation of the hapten--carrier protein-Ia antigen complex. In their absence in a large number of LC, following UV irradiation, epicutaneous application of a hapten would lead to the development of a state of immune tolerance.

Adenosine Triphosphatases↗
PubMed1994

The process of cellular uptake of iron from transferrin. A computer simulation program.

In an attempt to improve our understanding of the complex interplay between cell compartments and chemical species during cellular uptake of iron from transferrin, we designed a computer simulation program based on current models of receptor-mediated endocytosis and pinocytosis. The program calculates and visualizes, as a function of time, the changes in transferrin, apotransferrin, and iron concentrations occurring in all relevant cellular compartments during cellular iron acquisition from transferrin. Simulation of literature data showed that the program generates results that are in accordance with experimental data. Furthermore, from measurements of the uptake of [carboxyl-14C]dextran we could utilize the program to suggest rate constants characteristic for the pinocytic process in rat reticulocytes. Moreover, simulations indicate that the apparent difference in the iron uptake process observed between reticulocytes and hepatocytes may be explained by the contribution made by pinocytosis to the iron uptake process. Finally, the present program should have potential as an educational tool during introduction to the field of receptor-mediated endocytosis in general and to cellular iron metabolism in particular.

Animals↗
PubMed2006

Src triggers circular ruffling and macropinocytosis at the apical surface of polarized MDCK cells.

We addressed the role of Src on cortical actin dynamics and polarized endocytosis in MDCK cells harboring a thermosensitive v-src mutant. Shifting monolayers established at 40 degrees C (non-permissive temperature) to 34 degrees C (permissive temperature) rapidly reactivated v-Src kinase, but tight junctions and cell polarity resisted for >6 h. At this interval, activated v-src was recruited on apical vesicles, induced cortactin-associated apical circular ruffles productive of macropinosomes, thereby accelerating apical pinocytosis by approximately fivefold. Ruffling and macropinosome formation were selectively abrogated by inhibitors of actin polymerization, phosphoinositide 3-kinase, phospholipase C, and phospholipase D, which all returned apical pinocytosis to the level observed at 40 degrees C, underscoring the distinct control of apical micropinocytosis and macropinocytosis. Src promoted microtubule-dependent fusion of macropinosomes to the apical recycling endosome (ARE), causing its strong vacuolation. However, preservation of tubulation and apical polarity indicated that its function was not affected. The ARE was labeled for v-src, Rab11, and rabankyrin-5 but not early endosome antigen 1, thus distinguishing two separate Rab5-dependent apical pathways. The mechanisms of Src-induced apical ruffling and macropinocytosis could shed light on the triggered apical enteroinvasive pathogens entry and on the apical differentiation of osteoclasts.

Animals↗
PubMed1975

The effect of cyclophosphamide, methotrexate and X-irradiation on the ultrastructure and endocytic capacity of murine peritoneal macrophages.

100 mg/kg cyclophosphamide given subcutaneously daily for 5 days and whole-body X-irradiation (500 r) had an appreciable effect on the phagocytosis of E. coli by mouse peritoneal macrophages. Less bacteria were ingested by cells from the treated mice as compared with control cells. In contrast, whole-body X-irradiation had a stimulatory effect on pinocytosis as compared with cells from cyclophosphamide treated mice or control mice. Morphological changes in the cells from animals treated with cyclophosphamide or X-rays were evident. The cells were larger than normal macrophages and contained large amounts of lipid and phagolysosomes and had more vacuoles as compared with control cells. Many giant cells were present in the treated mice. Treatment of mice with methotrexate for 5 days, although affecting the cells morphologically in that they were larger than normal cells and had many vacuoles did not appear to have any effect on either phagocytosis or pinocytosis. Cells from methotrexate treated animals did not contain the large quantities of lipid seen in cells from the cyclophosphamide treated and X-irradiated mice.

Animals↗
PubMed1976

Uptake of diphtheria toxin and its fragment A moiety by mammalian cells in culture.

Evidence suggesting that diphtheria toxin reaches the cytoplasm of susceptible mammalian cells by two independent mechanisms is presented. A schematic model describing the two processes of toxin entry into the cell is developed. One process of toxin uptake considered to by physiologically significant is passage of the protein toxin through the plasma membrane. This most likely happens by binding of fragment B to receptors on the membrane and by subsequent toxin-membrane interaction so that ultimately fragment A, the enzymatically active moiety, is transported tothe cell interior. This process, which ultimately leads to cessation of protein synthesis and cell death, involves a comparatively small number of toxin molecules. A second mechanism of toxin uptake is by classical pinocytosis. The majority of toxin taken into the cell is accomplished by this process. The fate of toxin taken into HEp-2 cells via pinocytosis is proteolysis by lysosomal enzymes. Thus, such vesicle-bound toxin is ordinarily not expressed biologically. Evidence suggesting that ammonium chloride provides total protection to diphtheria toxin-susceptible cells by preventing entry of toxin by the specific receptor-associated process is also provided; data showing that the ammonium salt immobilizes bound toxin on the plasma membrane of HEp-2 cells are presented. Finally, it is suggested that actively endocytic cells such as guinea pig macrophages interact with toxin in a significantly different manner than do nonphagocytic cells.

Ammonium Chloride↗
PubMed1991

Endocytic mechanisms utilized by chlamydiae and their influence on induction of productive infection.

The microfilament-disrupting drug cytochalasin D and, initially, inoculation at 20 degrees C were used to differentiate between phagocytosis (sensitive to both treatments) and pinocytosis (resistant to both treatments) to assess whether chlamydial uptake into McCoy cells occurred by one or both mechanisms and whether each could contribute to productive infection. Both treatments suppressed the infectivity of Chlamydia trachomatis L2/434/Bu and C. psittaci GPIC (the guinea pig inclusion conjunctivitis strain) following static inoculation by only 50%, indicating that there was simultaneous operation of both phagocytosis and pinocytosis during uptake that led to productive infection. Measurement of the entry of organisms by two separate assays established that both strains predominantly used a cytochalasin D-resistant (pinocytic) mechanism, implying that phagocytic uptake was coupled to a higher frequency of productive infection. Integration of the data on infectivity and entry allowed the potential for an organism to infect a host cell to be quantified. This synthesis revealed that for both strains the infectivity potential following phagocytic entry was ca. 10-fold greater than that following pinocytic entry. However, both entry mechanisms were exploited more efficiently by strain L2/434/Bu than by strain GPIC (unless the latter was inoculated with centrifugation), indicating that intrinsic strain properties are more important for infectivity potential than the endocytic mechanism utilized.

Cell Line↗
PubMed1997

Involvement of p21racA, phosphoinositide 3-kinase, and vacuolar ATPase in phagocytosis of bacteria and erythrocytes by Entamoeba histolytica: suggestive evidence for coincidental evolution of amebic invasiveness.

Trophozoites of Entamoeba histolytica, the protozoan parasite that causes amebic dysentery, phagocytose bacteria in the colonic lumen and erythrocytes (RBC) in host tissues. Because tissue invasion is an evolutionary dead end, it is likely that amebic pathogenicity is coincidentally selected, i.e., the same methods used to kill bacteria in the colonic lumen are used by parasites to damage host cells and cause disease. In support of this idea, the amebic lectin and pore-forming peptide are involved in binding and killing, respectively, bacteria and host epithelial cells. Here amebic phagocytosis of bacteria, RBC, and mucin-coated beads was disrupted by overexpression of E. histolytica p21(racA-V12), a ras-family protein involved in selection of sites of actin polymerization, which had been mutated to eliminate its GTPase activity. p21(racA-V12) transformants were also defective in capping and cytokinesis, while pinocytosis of fluorescent dextrans was not affected. Wortmannin, a fungal inhibitor of phosphoinositide 3-kinase, markedly inhibited phagocytosis of bacteria, RBC, and mucin-coated beads by wild-type amebae. In contrast to p21(racA-V12) overexpression, wortmannin abolished amebic pinocytosis of dextrans but had no inhibitory effects on capping. Inhibition of amebic vacuolar acidification by bafilomycin also decreased bacterial and RBC uptake. These results, which demonstrate similarities between mechanisms of phagocytosis of bacteria and RBC by amebae and macrophages, support the idea of coincidental selection of amebic genes encoding proteins that mediate destruction of host cells.

Ammonium Chloride↗
PubMed2006

Efficient translocation of EspC into epithelial cells depends on enteropathogenic Escherichia coli and host cell contact.

EspC is an autotransporter protein secreted by enteropathogenic Escherichia coli (EPEC). The pathogenic role of EspC in EPEC infection is unknown. We have shown that the purified EspC produces enterotoxicity and cytotoxicity; for the latter effect, EspC must be internalized. However, the internalization mechanism is unknown. Here we show that azithromycin (an inhibitor of pinocytosis), but not drugs affecting caveole-, clathrin-, or receptor-mediated endocytosis, inhibited purified EspC internalization and cytoskeletal disruption, suggesting that purified EspC is internalized by pinocytosis. Furthermore, unlike in cholera toxin, we were unable to detect a receptor on epithelial cells by pretreatment at 4 degrees C. Upon EspC entry, it is delivered directly into the cell cytosol, as shown by the fact that drugs that inhibit intracellular trafficking had no effect on cytoskeletal disruption. All these data suggest that purified EspC internalization is not a physiological internalization mechanism; hence, we explored EspC internalization during the infection of epithelial cells by EPEC. Like other EPEC virulence factors, EspC secretion is stimulated by EPEC when it is grown in cell culture medium and enhanced by the presence of epithelial cells. Physiologically secreted EspC was efficiently internalized during EPEC and host cell interaction. Additionally, the lack of EspC internalization caused by using an isogenic mutant prevented the cytopathic effect caused by EPEC. These data suggest that EPEC uses an efficient mechanism to internalize milieu-secreted EspC into epithelial cells; once inside the cells, EspC is able to induce the cytopathic effect caused by EPEC.

Bacterial Adhesion↗
PubMed1982

Macrophage phagocytosis: analysis of particle binding and internalization.

An improved radioassay for analysis of phagocytosis has been used to quantitate and characterize the binding and internalization of zymosan by monolayers of rabbit pulmonary alveolar macrophages. This method distinguishes zymosan particles reversibly bound to the cell surface from those internalized. The zymosan was radiolabeled with technetium 99m(99mTc), a gamma-emitter with a 6-h half-life. Use of 99mTc as the radiolabel also permitted simultaneous determinations of pinocytosis and cellular protein content using [14C]sucrose and [3H]amino acids, respectively. All endocytic data were normalized per adherent cell based on this latter measurement. A significant fraction of the cell-associated particles was bound to the cell surface but not internalized. Failure to correct for this compartment would have resulted in overestimation of phagocytic rate and total cellular capacity. Both binding and ingestion of functionally unopsonized zymosan were found to be saturable, temperature sensitive, dependent on glycolytic energy, dependent on a trypsin-sensitive membrane component, described by a maximal rate, and limited by a finite capacity. The time courses of both processes were found to be similar. These results led us to conclude that, in our system, both binding and internalization were active processes and that the limited capacity to ingest zymosan was not explained by a concomitant reduction in binding of the particle to the cell membrane. Furthermore, it was found that phagocytosis did not change the rate of fluid-phase pinocytosis, consistent with the concept that the cell membrane is a functional mosaic as has been previously found by others for phagocytic and transport sites in this cell type.

Amino Acids↗
PubMed1984

Modulation of the blood-brain barrier permeability in neonatal cytotoxic brain edema: laboratory and morphological findings obtained on newborn piglets with experimental pneumothorax.

Acute, bilateral pneumothorax (PT) was produced in 14 newborn piglets. The clinical status of the operated and 14 control animals was monitored by measuring the arterial blood gases, acid-base balance and mean arterial blood pressure. Different brain regions were processed for electron microscopy and albumin immunohistochemistry; water and electrolyte contents were also determined at the end stage of experimental intervention. Electron microscopy showed more intense pinocytotic activity in the endothelium of brain capillaries from PT animals evaluated by morphometry. Statistically significant (p less than 0.01) differences were found in the distribution of pinocytotic vesicles in different brain areas of PT animals. The blood-brain barrier seemed to be impermeable to albumin in all brain regions both in the controls and in the PT group. Parallel with the changes observed in pinocytosis, the water and sodium contents were also increased in the PT group in the parietal cortex (water content 85.18 +/- SD 0.81% vs. 84.10 +/- SD 0.52%, p less than 0.01; sodium content in wet brain tissue 70.94 +/- SD 8.44 mmol/kg vs. 65.09 +/- SD 4.43 mmol/kg, p less than 0.05, in dry brain tissue 481.70 +/- 75.70 mmol/kg vs. 410.15 +/- SD 35.45 mmol/kg, p less than 0.05) and in the cerebellum (water content 83.95 +/- SD 1.08% vs. 83.02 +/- SD 0.89%, p less than 0.05; sodium content in wet brain tissue 60.67 +/- SD 3.16 mmol/kg vs. 55.90 +/- 6.26 mmol/kg, p less than 0.01). However, in other brain regions--especially in the water-shed area--there was no correlation between the changes of pinocytosis and water-electrolyte contents of the tissues. It is suggested that the type of edema developing in this severe cardiovascular/hypoxic collapse is cytotoxic of origin and this fact should be more seriously taken into account in the treatment of the disease.

Animals↗
PubMed1982

Temperature dependence of certain integrated membrane functions in macrophages.

We have studied the effect of temperature on uptake and degradation of molecules entering mouse peritoneal macrophages by fluid-phase, adsorptive and receptor-mediated pinocytosis, and on degradation of their intracellular proteins. Uptake of [3H]sucrose and uptake and degradation of formaldehyde-treated 125I-labelled human serum albumin and 125I-labelled mannose-bovine serum albumin continued, but were progressively slowed as the temperature decreased from 37 degrees C to 20 degrees C. The uptake and degradation were completely abolished at approximately 15 degrees C. Arrhenius plots for adsorptive and fluid uptake were unilinear, whereas that for receptor-mediated endocytosis showed an inflection point at approximately 20 degrees C. The results did not indicate any distinction between adsorptive and fluid pinocytosis. An 'intracellular turnover time' calculated for mannose-bovine serum albumin taken up by the specific route is 19-24 min and this time calculated for human serum albumin is, in contrast, 99 min. Studies of the kinetics of degradation of both endocytosed and endogenous proteins showed similarity in the temperature cut-off of degradation of endocytosed and endogenous long-half-life proteins (congruent to 15 degrees C) and continuance of endogenous short-half-life degradation at much lower temperatures.

Animals↗