Home About us Contact
|
Home About us Contact | ||
|
|
||
II Cells (ii + cell)
Kinds of II Cells Selected AbstractsEffect of Chronic Ethanol Ingestion on Alveolar Type II Cell: Glutathione and Inflammatory Mediator-Induced ApoptosisALCOHOLISM, Issue 7 2001Lou Ann S. Brown Background : In septic patients, chronic alcohol abuse increases the incidence of the acute respiratory distress syndrome, a syndrome that requires alveolar type II cell proliferation and differentiation for repair of the damaged alveolar epithelium. We previously showed in a rat model that chronic ethanol ingestion decreased the antioxidant glutathione (GSH) in type II cells and exacerbated endotoxin-mediated acute lung injury. We hypothesized that this GSH depletion by ethanol, particularly mitochondrial GSH, predisposed type II cells to inflammatory mediator-induced apoptosis. Methods: Adult male rats were fed the Lieber-DeCarli diet for 2, 6, or 16 weeks. Alveolar type II cells were then isolated and treated with hydrogen peroxide or TNF-,. The effect on glutathione (cytosolic and mitochondrial), apoptotic events, and necrosis were determined. In other studies, rats were fed ethanol for 6 weeks and were treated with endotoxin and apoptosis of type II cells determined by the TUNEL method. Results: Chronic ethanol ingestion alone resulted in a progressive decrease in mitochondrial GSH and a progressive increase in the basal apoptosis and necrosis rate (p, 0.05). Furthermore, there was a progressive increase in the sensitivity of the cells to H2O2 or TNF-, induced cytochrome c release, caspase 3 activation, apoptosis, and necrosis (p, 0.05). Finally, there was a 2-fold increase in apoptotic type II cells in vivo when chronic ethanol ingestion was superimposed on endotoxemia. Conclusions: These results suggested that chronic ethanol ingestion resulted in a progressive depletion of mitochondrial GSH and sensitization of type II cells to inflammatory mediator-induced apoptosis and necrosis. These effects may be particularly relevant during acute stress when proliferation and differentiation of these cells are critical to repair of the damaged alveolar epithelium and may have important ramifications for the treatment of acute respiratory distress syndrome in patients with a history of alcohol abuse. [source] ,-tocopherol improves impaired physiology of rat type II pneumocytes isolated from experimentally injured lungsEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 11 2000B. Müller Background Oxidant stress delivered by nitrogen dioxide (NO2) inhalation impairs the function of extracellular surfactant as well as surfactant phospholipid metabolism in type II pneumocytes. Because protection against oxidant stress is important to normal lung function, the lung contains a variety of antioxidants, including vitamin E. Whether administration of this antioxidant during NO2 inhalation attenuates NO2 -induced alterations in phospholipid metabolism in type II pneumocytes has not been studied. Methods We exposed rats to identical NO2 body doses (720 p.p.m. x h) using continuous, intermittent, or repetitive protocols. During exposure periods, the animals received daily intramuscular injections of vitamin E (25 mg kg,1). We isolated type II pneumocytes from NO2 -exposed rats and evaluated them for cell yield and viability, as well as for synthesis and secretion of phosphatidylcholine (PC) as measures of surfactant metabolism. Results The yield of type II pneumocytes was significantly elevated from animals that had been exposed continuously to NO2 whereas in intermittently and repeatedly exposed rats, cell yield was similar to yield from control animals. Viability of the isolated cells was similar in controls and all NO2 exposure protocols. Vitamin E treatment of the NO2 -exposed rats neither changed cell yield nor cell viability. Phospholipid de novo synthesis, as estimated by choline incorporation into PC, was increased most after continuous NO2 inhalation whereas in the other conditions there was only a slight increase. Vitamin E administration further increased phospholipid synthesis; this difference reached statistical significance only in the case of intermittent NO2 exposure. Secretion of phosphatidylcholine from type II cells was only reduced after continuous NO2 inhalation and administration of the antioxidant reduced the impairment. Conclusion Because vitamin E appears to preserve the ability of type II pneumocytes isolated from NO2 -exposed rats to synthesize and secrete surfactant lipid, we conclude that administration of vitamin E may mitigate NO2 -induced lung injury. [source] Immunophenotypic discrepancies between granulocytic and erythroid lineages in peripheral blood of patients with paroxysmal nocturnal haemoglobinuriaEUROPEAN JOURNAL OF HAEMATOLOGY, Issue 1 2000Kriangsak Pakdeesuwan Abstract: In paroxysmal nocturnal haemoglobinuria (PNH), somatic mutation of the PIG-A gene is thought to result in altered expression of glycosylphosphatidylinositol (GPI)-anchored proteins. This study was performed to determine if there were any heterogeneities of cellular phenotypes between two major peripheral blood cells, erythrocytes and granulocytes. Using CD59-based immunocytometry, the patterns of CD59 expression were shown to be conserved in the circulating erythroid cells (reticulocytes and mature erythrocytes) in all 29 patients with PNH. Twenty-one patients had distinct combinations of PNH type I, II, and III cells in different lineages. Only eight patients exhibited similar patterns of CD59 expression between the two lineages. Approximately one third of the patients had PNH type II cells in either or both of the two lineages indicating variable lineage involvement. The proportion of abnormal granulocutes was higher than those of abnormal reticulocytes and erythrocytes. In patients with appropriate erythropoietic responses to haemolysis (RPI>2.0), shift reticulocytes display predominantly PNH phenotypes. These immature erythroid cells with altered expression of GPI-anchored proteins may dominate the peripheral blood during periods of increased marrow activity resulting in greater phenotypic mosaicism in such patients. Discrepancies in expression of GPI-anchored proteins in PNH which are highly variable between the two lineages may be the result of their different life spans and the influence of complement-mediated cytolysis. The phenomena also indicated the possible occurrence of more than one PNH clones with variable clonal dominance. [source] Cell shrinkage evoked by Ca2+ -free solution in rat alveolar type II cells: Ca2+ regulation of Na+,H+ exchangeEXPERIMENTAL PHYSIOLOGY, Issue 2 2005Hitoshi Murao The effects of intracellular Ca2+ concentration, [Ca2+]i, on the volume of rat alveolar type II cells (AT-II cells) were examined. Perfusion with a Ca2+ -free solution induced shrinkage of the AT-II cell volume in the absence or presence of amiloride (1 ,m, an inhibitor of Na+ channels); however, it did not in the presence of 5-(N -methyl- N -isobutyl)-amiloride (MIA, an inhibitor of Na+,H+ exchange). MIA decreased the volume of AT-II cells. Inhibitors of Cl,,HCO3, exchange, 4,4,-diisothiocyanostilbene-2,2,-disulfonic acid (DIDS) and 4-acetamido-4,-isothiocyanatostilbene-2,2,-disulfonic acid (SITS) also decreased the volume of AT-II cells. This indicates that the cell shrinkage induced by a Ca2+ -free solution is caused by a decrease in NaCl influx via Na+,H+ exchange and Cl,,HCO3, exchange. Addition of ionomycin (1 ,m), in contrast, induced cell swelling when AT-II cells were pretreated with quinine and amiloride. This swelling of the AT-II cells is not detected in the presence of MIA. Intracellular pH (pHi) measurements demonstrated that the Ca2+ -free solution or MIA decreases pHi, and that ionomycin increases it. Ionomycin stimulated the pHi recovery after an acid loading (NH4+ pulse method), which was not noted in MIA-treated AT-II cells. Ionomycin increased [Ca2+]i in fura-2-loaded AT-II cells. In conclusion, the Na+,H+ exchange activities of AT-II cells, which maintain the volume and pHi, are regulated by [Ca2+]i. [source] Repertoire selection by pre-B-cell receptors and B-cell receptors, and genetic control of B-cell development from immature to mature B cellsIMMUNOLOGICAL REVIEWS, Issue 1 2000Fritz Melchers Summary: During B-cell development the surrogate light (SL) chain is selectively expressed in progenitor and precursor B cells during the developmental stages of DH to JH and VH to DH JH rearrangements. Approximately half of all H chains produced by these rearrangements cannot pair with SL chains and cannot form a pre-B-cell receptor (pre-BCR). A spectrum of affinities between VpreB and individual VH domains generates preB cells with pre-BCR of different fitness which, in turn, determines the extent of the pre-B II-cell proliferation and the fidelity of allelic exclusion of the H chain locus. Once pre-BCR is expressed, SL chain expression is turned off. As pre-B II cells proliferate, SL is diluted out, thus limiting pre-BCR formation. As a consequence, pre-B II cells stop proliferating, become small and resting and begin to rearrange the L chain loci. Multiple rearrangements of the k L chain alleles are often detected in wild-type small pre-B II cells. Around 20% of the H chain-expressing small pre-B II cells also express L chains but do not display the Ig on the surface. Hence, it is likely that not all L chains originally generated in resting pre-B II cells can pair with the H chain previously present in that cell. The best fitting ones are selected preferentially to generate sIg+ B cells. Furthermore, the transition of immature B cells from the bone marrow to spleen and their development to mature cells appear as two separate steps controlled by different genes. [source] Prolactin secretion and intracellular Ca2+ change in rat lactotroph subpopulations stimulated by thyrotropin-releasing hormone,JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 2 2002Chih-Yang Huang Abstract Thyrotropin-releasing hormone (TRH) may stimulate lactotrophs to increase intracellular Ca2+ and to secrete prolactin (PRL). In this study, PRL contents in lactotrophs were determined by the sequential cell immunoblot assay (SCIBA) and their changes in intracellular Ca2+ was analyzed by confocal microscopy. Significant correlations were found in the corresponding parameters between TRH treatments with a recovery interval of 2 h. Measuring the PRL contents after the first TRH treatment and then determining the intracellular Ca2+ changes after the second TRH treatment revealed four lactotroph subpopulations. Type I cells (51%) showed significant responses of both PRL secretion and intracellular Ca2+ concentration. Type II cells (22%) increased in PRL secretion, but without changes in intracellular Ca2+. Type III cells (17%) have increased in intracellular Ca2+, but without changes in PRL secretion. Type IV cells (10%) did not show changes in PRL secretion and intracellular Ca2+. J. Cell. Biochem. 87: 126,132, 2002. © 2002 Wiley-Liss, Inc. [source] Differential expression of voltage-activated calcium currents in zebrafish retinal ganglion cellsJOURNAL OF NEUROSCIENCE RESEARCH, Issue 3 2006Luoxiu Huang Abstract We report a study on the characterization of voltage-activated calcium currents (ICa) in retinal ganglion cells (RGCs) and the topographic distribution of RGCs that express different types of ICa in zebrafish retinas. In acutely isolated zebrafish RGCs, both high-voltage-activated (HVA; peak activation potential +7.4 ± 1.1 mV) and low-voltage-activated (LVA; peak activation potential ,33.0 ± 1.2 mV) ICa were recorded. HVA ICa were recorded in all of the tested RGCs, whereas LVA ICa were recorded in approximately one-third of the tested cells. In RGCs that expressed both HVA and LVA ICa, the two currents were readily separated by depolarizing the cell membrane to different voltages from different holding potentials. Among RGCs that expressed LVA ICa, some cells expressed large LVA ICa (up to 130 pA), whereas others expressed small LVA ICa (approximately 20 pA). RGCs that expressed large and small LVA ICa were designated as class I and class II cells, respectively, and RGCs that expressed only HVA ICa were designated as class III cells. The topographic distribution of cell classes was similar in various areas of the retina. In the nasal-ventral retina, for example, class III cells outnumbered class I and class II cells by 10.8- and 2.6-fold, respectively. In the temporal and dorsal retinas, the density of class III cells slightly decreased, whereas the density of class I and class II cells increased. The differential expression of ICa in RGCs may correlate with the development and function of the retina. © 2006 Wiley-Liss, Inc. [source] Alcohol Primes the Airway for Increased Interleukin-13 SignalingALCOHOLISM, Issue 3 2009Patrick O. Mitchell Background:, Using an experimental model of airway fibrosis following lung transplantation, we recently showed that chronic alcohol ingestion by donor rats amplifies airway fibrosis in the recipient. Associated with alcohol-mediated amplification of airway fibrosis is increased transforming growth factor ,-1(TGF,1) and ,-smooth muscle actin expression. Other studies have shown that interleukin-13 (IL-13) modulates TGF,1 signaling during experimentally-induced airway fibrosis. Therefore, we hypothesized that IL-13 is a component of alcohol-mediated amplification of pro-fibrotic mediators in the alcoholic lung. Methods:, To test this hypothesis, we analyzed tracheal epithelial cells and type II alveolar cells from control- or alcohol-fed rats, alcohol-treated mouse lung fibroblasts, and human bronchial epithelial cells in vitro for expression of various components of the IL-13 signaling pathway. Signaling via the IL-13 pathway was assessed by measuring levels of phosphorylated signal transducers and activators of transcription-6 (STAT6). In addition, we performed heterotopic tracheal transplantation using control-fed and alcohol-fed donor rats and analyzed tracheal allografts for expression of components of the IL-13 signaling pathway by RT-PCR and immunocytochemical analyses. Results:, Interleukin-13 expression was detected in type II alveolar epithelial cells and human bronchial epithelial cells, but not in lung fibroblasts. IL-13 expression was decreased in whole lung and type II cells in response to alcohol exposure. In all cell types analyzed, expression of IL-13 signaling receptor (IL-13R,1) mRNA was markedly increased. In contrast, mRNA and protein expression of the IL-13 decoy receptor (IL-13R,2) were decreased in all cells analyzed. Exposure to alcohol also increased STAT6 phosphorylation in response to IL-13 and lipopolysaccharide. Conclusions:, Data from multiple cell types in the pulmonary system suggest that IL-13 and its receptors play a role in alcohol-mediated activation of pro-fibrotic pathways. Taken together, these data suggest that alcohol primes the airway for increased IL-13 signaling and subsequent tissue remodeling upon injury such as transplantation. [source] Effect of Chronic Ethanol Ingestion on Alveolar Type II Cell: Glutathione and Inflammatory Mediator-Induced ApoptosisALCOHOLISM, Issue 7 2001Lou Ann S. Brown Background : In septic patients, chronic alcohol abuse increases the incidence of the acute respiratory distress syndrome, a syndrome that requires alveolar type II cell proliferation and differentiation for repair of the damaged alveolar epithelium. We previously showed in a rat model that chronic ethanol ingestion decreased the antioxidant glutathione (GSH) in type II cells and exacerbated endotoxin-mediated acute lung injury. We hypothesized that this GSH depletion by ethanol, particularly mitochondrial GSH, predisposed type II cells to inflammatory mediator-induced apoptosis. Methods: Adult male rats were fed the Lieber-DeCarli diet for 2, 6, or 16 weeks. Alveolar type II cells were then isolated and treated with hydrogen peroxide or TNF-,. The effect on glutathione (cytosolic and mitochondrial), apoptotic events, and necrosis were determined. In other studies, rats were fed ethanol for 6 weeks and were treated with endotoxin and apoptosis of type II cells determined by the TUNEL method. Results: Chronic ethanol ingestion alone resulted in a progressive decrease in mitochondrial GSH and a progressive increase in the basal apoptosis and necrosis rate (p, 0.05). Furthermore, there was a progressive increase in the sensitivity of the cells to H2O2 or TNF-, induced cytochrome c release, caspase 3 activation, apoptosis, and necrosis (p, 0.05). Finally, there was a 2-fold increase in apoptotic type II cells in vivo when chronic ethanol ingestion was superimposed on endotoxemia. Conclusions: These results suggested that chronic ethanol ingestion resulted in a progressive depletion of mitochondrial GSH and sensitization of type II cells to inflammatory mediator-induced apoptosis and necrosis. These effects may be particularly relevant during acute stress when proliferation and differentiation of these cells are critical to repair of the damaged alveolar epithelium and may have important ramifications for the treatment of acute respiratory distress syndrome in patients with a history of alcohol abuse. [source] ErbB receptor dimerization, localization, and co-localization in mouse lung type II epithelial cells,PEDIATRIC PULMONOLOGY, Issue 12 2006Katja Zscheppang MSc Abstract ErbB receptors are crucial for embryonic neuronal and cardiac development. ErbB receptor ligands neuregulin (NRG) and epidermal growth factor (EGF) play a major role in the developing lung, specifically in mesenchymal induced fetal surfactant synthesis by type II epithelial cells. Different erbB receptor ligands cause diverse biologic effects by stimulating specific erbB-dimers. It is not known how dimerization, cellular localization, and co-localization of erbB dimers are regulated in type II epithelial cells. We hypothesized that erbB receptors have a distinct dimerization, localization, and co-localization pattern in type II cells. In mouse type II epithelial cells, which express all four erbB receptors, erbB1 and erbB4 were the preferred dimerization partners. These dimerization patterns were ligand independent. Confocal microscopy showed these transmembrane receptors exhibited a strong nuclear localization. In non-stimulated cells, both erbB1 and erbB2 were predominantly localized to the nucleus and less intensely to the cytoplasm. However, erbB1 was mainly found in the nucleoli, whereas erbB2 spared the nucleolar region. ErbB3 was exclusively located in the nucleoli. ErbB4 was diffusely located in nucleus and cytoplasm, and like erbB2 spared the nucleolar region. Short stimulation with either EGF or NRG led to a more pronounced nuclear staining for erbB1, erbB2, and erbB4. All four receptors co-localized with each other after stimulation, but with varying intensity. The two known stimulators of fetal surfactant synthesis, NRG and NRG-containing fibroblast conditioned medium, changed cellular localization of the dimerization partners erbB4 and erbB2 in a distinct fashion. We conclude that erbB receptors have a receptor-specific localization and dimerization pattern in type II epithelial cells. Pediatr Pulmonol. 2006; 41:1205,1212. © 2006 Wiley-Liss, Inc. [source] Glycinergic input of widefield, displaced amacrine cells of the mouse retinaTHE JOURNAL OF PHYSIOLOGY, Issue 15 2009Sriparna Majumdar Glycine receptors (GlyRs) of displaced amacrine cells of the mouse retina were analysed using whole cell recordings and immunocytochemical staining with subunit-specific antibodies. During the recordings the cells were filled with a fluorescent tracer and 11 different morphological types could be identified. The studies were performed in wild-type mice and in mutant mice deficient in the GlyR,1 (Glra1spd-ot, ,oscillator' mouse), the GlyR,2 (Glra2,/,) and the GlyR,3 subunit (Glra3,/,). Based on their responses to the application of exogenous glycine in the retinas of wild-type and mutant mice, the cells were grouped into three major classes: group I cells (comprising the morphological types MA-S5, MA-S1, MA-S1/S5, A17, PA-S1, PA-S5 and WA-S1), group II cells (comprising the morphological types PA-S4, WA-S3 and WA-multi) and ON-starburst cells. For further analysis, spontaneous inhibitory postsynaptic currents (sIPSCs) were measured both in wild-type and mutant mouse retinas. Glycinergic sIPSCs and glycine induced currents of group I cells remained unaltered across wild-type and the three mutant mice (mean decay time constant of sIPSCs, ,,25 ms). Group II cells showed glycinergic sIPSCs and glycine induced currents in wild-type, Glra1spd-ot and Glra3,/, mice (,,25 ms); however, glycinergic currents were absent in group II cells of Glra2,/, mice. Glycine induced currents and sIPSCs recorded from ON-starburst amacrine cells did not differ significantly between wild-type and the mutant mouse retinas (,,50,70 ms). We propose that GlyRs of group II cells are dominated by the ,2 subunit; GlyRs of ON-starburst amacrine cells appear to be dominated by the ,4 subunit. [source] Scanning Electron Microscopy of the Orbital Harderian Gland in the Male Atlantic Bottlenose Dolphin (Tursiops truncatus)ANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 4 2009G. G. Ortiz Summary The ultrastructure of the Harderian gland of Atlantic bottlenose dolphin (Tursiops truncatus) was examined by scanning electron microscopy (SEM). We found the following surface features: the typical round appearance of the ascinar glandular unit with a finely granular surface, a thin cortex and immediately below two types of cells: type I cells (characterized by small lipid vacuoles) and type II cells (characterized by large lipid vacuoles). It has been suggested that different cells forms represent a single cell type in varying activity states. Additionally, a coalescent tubular complex, a small balloon-like structures and large globular structures were observed. These structures may be reservoirs of secretion products. [source] Distribution and Cytoarchitecture of Sympathetic Neurons Innervating the Pineal Gland in Chick: A CTB-HRP StudyANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 1 2009L. Jia Summary The neurons in bilateral superior cervical ganglia (SCG) innervating the chick pineal gland were labelled by using the technique of retrograde axonal labelling with cholera toxin B subunit linked to horseradish peroxidase (CTB-HRP). To our results, perikarya of these sympathetic neurons distributed from rostral to caudal in the SCG, and mainly localized in the opposite side of the paravertebral trunk. The fibres of these neurons were collected by the cephalic carotid nerve. According to the sizes of somal area and dendritic field, these sympathetic neurons projecting to the pineal gland were classified into four major groups: group I cells (52.4%) with a small somal area (303.5 ,m2 on average) and narrow dendritic field (3767.8 ,m2 on average), group II cells (39.0%) with a middle-sized somal area (473.3 ,m2) and middle-sized dendritic field (7522.2 ,m2), group III cells (6.4%) with a middle-sized somal area (473.4 ,m2) and wide dendritic field (13 104.4 ,m2), and group IV cells (2.2%) with a large somal area (940.7 ,m2) and wide dendritic field (14 553.2 ,m2). Of these pineal projecting neurons, most took on a lesser dendritic field. The neurons with small or middle-sized dendritic field from group I and II were about 91.4% of the total neurons labelled with CTB-HRP, and the neurons with wide dendritic field from group III and IV were less with 8.6%. [source] | |||||||||||||