Relevant bibliographies by topics / Pneumocyty

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Pneumocyty'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Pneumocyty"

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Rekhtman, Natasha. "“Napoleon Hat” Sign: A Distinctive Cytologic Clue to Reactive Pneumocytes." Archives of Pathology & Laboratory Medicine 144, no. 4 (2020): 443–45. http://dx.doi.org/10.5858/arpa.2019-0615-sa.

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Various types of acute and subacute lung injury can cause severe reactive pneumocyte atypia, which may mimic malignant proliferations and present a major diagnostic pitfall. This particularly applies to cytologic preparations and frozen sections, where background inflammatory injury may be subtle or not apparent. Although several distinguishing morphologic features of reactive pneumocytes have been suggested, there is significant overlap with neoplastic proliferations. In this article, a highly distinctive but underrecognized feature of reactive pneumocytes is highlighted that can serve as a useful diagnostic clue. The feature refers to the distinctive pinched shape of reactive pneumocytes, for which the author has coined the term “Napoleon hat” sign to draw the analogy with the iconic headwear. The analogy vividly captures the distinctive shape of reactive pneumocytes, and can serve as a useful diagnostic and teaching tool in the interpretation of pulmonary specimens.
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Buch, S., R. N. Han, J. Liu, et al. "Basic fibroblast growth factor and growth factor receptor gene expression in 85% O2-exposed rat lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 268, no. 3 (1995): L455—L464. http://dx.doi.org/10.1152/ajplung.1995.268.3.l455.

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Lungs exposed to elevated O2 concentrations suffer an initial loss of type I pneumocytes, followed by a reparative type II pneumocyte hyperplasia. We hypothesized that type II pneumocyte hyperplasia after exposure of young adult rats to 85% O2 in vivo would be temporally related to 1) an increased concentration of intrapulmonary basic fibroblast growth factor (bFGF), a potent stimulator of type II pneumocyte DNA synthesis in vitro, and 2) an upregulation of pneumocyte receptors for bFGF (FGF-R). Increased rat lung bFGF mRNA, relative to air-exposed control animals, was observed at 4 days of exposure, with no increase at days 6 and 14 of exposure. Parallel changes were observed with bFGF receptor (flg) mRNA. Nuclear runoff assays confirmed increased transcription of both bFGF and flg genes in response to 85% O2, whereas increased translation at 6 days of exposure was confirmed by protein immunoanalysis. Immunohistochemistry demonstrated a broad distribution of bFGF throughout the lung, including the alveolar epithelium, which increased after 6 and 14 days of exposure to 85% O2. Our findings are compatible with a role for bFGF in O2-mediated pneumocyte hyperplasia.
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Tanswell, A. K., P. J. Byrne, R. N. Han, J. D. Edelson, and V. K. Han. "Limited division of low-density adult rat type II pneumocytes in serum-free culture." American Journal of Physiology-Lung Cellular and Molecular Physiology 260, no. 6 (1991): L395—L402. http://dx.doi.org/10.1152/ajplung.1991.260.6.l395.

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A previously reported serum-free medium for the culture of adult rat type II pneumocytes has been further defined by the addition of 10 mM N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid buffer and 700 U/ml catalase. Both additions significantly enhanced [3H]thymidine incorporation into pneumocyte DNA between days 5 and 6 of culture. In the presence of 100 micrograms/ml bovine pituitary extract, both insulin-like growth factor (IGF) I (20 ng/ml) and II (25 ng/ml) further increased [3H]thymidine incorporation into pneumocyte DNA over that observed with the basal medium. When type II pneumocytes were plated at 2.75 X 10(5) cells/cm2 there was a plating efficiency of 50 +/- 5%, and the increased DNA synthesis in response to IGFs was not associated with an increase in cell number. When the plating number was reduced to 1.6 X 10(5) cells/cm2 the plating efficiency was only 23 +/- 2%. At this low cell density a doubling of cell number was observed in response to IGF-I between days 4 and 9 of culture.
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Yamada, Tsutomu, and Yoshinori Kawabata. "Pneumocyte injury and ubiquitin‐positive pneumocytes in interstitial lung diseases." Histopathology 66, no. 2 (2014): 161–72. http://dx.doi.org/10.1111/his.12528.

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Kobayashi, T., K. Satoh, and M. Ohkawa. "Multifocal micronodular pneumocyte hyperplasia associated with tuberous sclerosis." Acta Radiologica 46, no. 1 (2005): 37–40. http://dx.doi.org/10.1080/02841850510020860.

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A case of multifocal micronodular pneumocyte hyperplasia (MMPH) associated with tuberous sclerosis is reported. MMPH is a rare pulmonary disorder characterized by the nodular proliferation of type II pneumocytes. In the case presented here, MMPH appeared as multiple, well‐defined small nodules with ground‐glass opacity. It is necessary to consider MMPH when small nodules with ground‐glass opacity are observed on HRCT in patients with tuberous sclerosis.
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Stevens, P. A., H. Wissel, D. Sieger, V. Meienreis-Sudau, and B. Rüstow. "Identification of a new surfactant protein A binding protein at the cell membrane of rat type II pneumocytes." Biochemical Journal 308, no. 1 (1995): 77–81. http://dx.doi.org/10.1042/bj3080077.

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Antibodies against a type II pneumocyte component were developed by an auto-anti-idiotypic approach using surfactant-associated protein A (SP-A) as the immunogen. The antibodies recognize an SP-A-binding protein (approximately 170-200 kDa under non-reducing conditions, 55 kDa under reducing conditions) on the cell membrane of rat type II pneumocytes. One of the antibodies competes with SP-A for binding to type II cells. In immunization assays in vitro, with this antibody as the antigen, anti-SP-A antibodies have been generated. The SP-A-binding cell membrane protein recognized by this auto-anti-idiotypic antibody may be involved in the interaction of extracellular SP-A with the type II pneumocyte and may play a role in the regulation of alveolar surfactant metabolism.
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Ji, Rong, Clement M. Lee, Linda W. Gonzales, et al. "Human type II pneumocyte chemotactic responses to CXCR3 activation are mediated by splice variant A." American Journal of Physiology-Lung Cellular and Molecular Physiology 294, no. 6 (2008): L1187—L1196. http://dx.doi.org/10.1152/ajplung.00388.2007.

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Chemokine receptors control several fundamental cellular processes in both hematopoietic and structural cells, including directed cell movement, i.e., chemotaxis, cell differentiation, and proliferation. We have previously demonstrated that CXCR3, the chemokine receptor expressed by Th1/Tc1 inflammatory cells present in the lung, is also expressed by human airway epithelial cells. In airway epithelial cells, activation of CXCR3 induces airway epithelial cell movement and proliferation, processes that underlie lung repair. The present study examined the expression and function of CXCR3 in human alveolar type II pneumocytes, whose destruction causes emphysema. CXCR3 was present in human fetal and adult type II pneumocytes as assessed by immunocytochemistry, immunohistochemistry, and Western blotting. CXCR3-A and -B splice variant mRNA was present constitutively in cultured type II cells, but levels of CXCR3-B greatly exceeded CXCR3-A mRNA. In cultured type II cells, I-TAC, IP-10, and Mig induced chemotaxis. Overexpression of CXCR3-A in the A549 pneumocyte cell line produced robust chemotactic responses to I-TAC and IP-10. In contrast, I-TAC did not induce chemotactic responses in CXCR3-B and mock-transfected cells. Finally, I-TAC increased cytosolic Ca2+ and activated the extracellular signal-regulated kinase, p38, and phosphatidylinositol 3-kinase (PI 3-kinase)/protein kinase B kinases only in CXCR3-A-transfected cells. These data indicate that the CXCR3 receptor is expressed by human type II pneumocytes, and the CXCR3-A splice variant mediates chemotactic responses possibly through Ca2+ activation of both mitogen-activated protein kinase and PI 3-kinase signaling pathways. Expression of CXCR3 in alveolar epithelial cells may be important in pneumocyte repair from injury.
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Winters, Christopher J., Olha Koval, Shubha Murthy, et al. "CaMKII inhibition in type II pneumocytes protects from bleomycin-induced pulmonary fibrosis by preventing Ca2+-dependent apoptosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 310, no. 1 (2016): L86—L94. http://dx.doi.org/10.1152/ajplung.00132.2015.

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The calcium and calmodulin-dependent kinase II (CaMKII) translates increases in intracellular Ca2+ into downstream signaling events. Its function in pulmonary pathologies remains largely unknown. CaMKII is a well-known mediator of apoptosis and regulator of endoplasmic reticulum (ER) Ca2+. ER stress and apoptosis of type II pneumocytes lead to aberrant tissue repair and progressive collagen deposition in pulmonary fibrosis. Thus we hypothesized that CaMKII inhibition alleviates fibrosis in response to bleomycin by attenuating apoptosis and ER stress of type II pneumocytes. We first established that CaMKII was strongly expressed in the distal respiratory epithelium, in particular in surfactant protein-C-positive type II pneumocytes, and activated after bleomycin instillation. We generated a novel transgenic model of inducible expression of the CaMKII inhibitor peptide AC3-I limited to type II pneumocytes (Tg SPC-AC3-I). Tg SPC-AC3-I mice were protected from development of pulmonary fibrosis after bleomycin exposure compared with wild-type mice. CaMKII inhibition also provided protection from apoptosis in type II pneumocytes in vitro and in vivo. Moreover, intracellular Ca2+ levels and ER stress were increased by bleomycin and significantly blunted with CaMKII inhibition in vitro. These data demonstrate that CaMKII inhibition prevents type II pneumocyte apoptosis and development of pulmonary fibrosis in response to bleomycin. CaMKII inhibition may therefore be a promising approach to prevent or ameliorate the progression of pulmonary fibrosis.
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Tanswell, A. K., D. M. Olson, and B. A. Freeman. "Liposome-mediated augmentation of antioxidant defenses in fetal rat pneumocytes." American Journal of Physiology-Lung Cellular and Molecular Physiology 258, no. 4 (1990): L165—L172. http://dx.doi.org/10.1152/ajplung.1990.258.4.l165.

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Cultured pneumocytes, prepared from fetal rat lung, are growth inhibited and have increased lactate dehydrogenase release and prostaglandin synthesis in response to 50 and 95% O2 exposure. The uptake of cationic liposomes by these fetal cells is more rapid and extensive than is the case with cultured adult pneumocytes. Protection of fetal pneumocytes against the cytotoxic effects of 50 or 95% O2 by liposome-entrapped antioxidant enzymes requires a liposome phospholipid concentration of only 1 nmol/cm2, compared with 45 nmol/cm2 for adult cells, which is a cytotoxic phospholipid concentration for the fetal cells. Despite this capacity of low concentrations of liposomes containing superoxide dismutase and catalase to increase endogenous antioxidant enzyme content, and to protect against cell death, such treatment does not attenuate O2-mediated alterations of cell growth or prostaglandin release. Inhibition of pneumocyte DNA synthesis, by elevated O2 concentrations, cannot be attributed to an autocrine effect of enhanced prostaglandin synthesis, because the addition of 50 microM ibuprofen to inhibit prostaglandin synthesis does not prevent O2-mediated effects on DNA synthesis.
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Kotton, Darrell N., Bei Yang Ma, Wellington V. Cardoso, et al. "Bone marrow-derived cells as progenitors of lung alveolar epithelium." Development 128, no. 24 (2001): 5181–88. http://dx.doi.org/10.1242/dev.128.24.5181.

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We assessed the capacity of plastic-adherent cultured bone marrow cells to serve as precursors of differentiated parenchymal cells of the lung. By intravenously delivering lacZ-labeled cells into wild-type recipient mice after bleomycin-induced lung injury, we detected marrow-derived cells engrafted in recipient lung parenchyma as cells with the morphological and molecular phenotype of type I pneumocytes of the alveolar epithelium. At no time after marrow cell injection, did we detect any engraftment as type II pneumocytes. In addition, we found that cultured and fresh aspirates of bone marrow cells can express the type I pneumocyte markers, T1α and aquaporin-5. These observations challenge the current belief that adult alveolar type I epithelial cells invariably arise from local precursor cells and raise the possibility of using injected marrow-derived cells for therapy of lung diseases characterized by extensive alveolar damage.
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Dissertations / Theses on the topic "Pneumocyty"

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Maker, Garth Lucas. "Regulation of surfactant production by fetal type II pneumocytes and characterization of fibroblast-pneumocyte factor /." Access via Murdoch University Digital Theses Project, 2007. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20080430.141113.

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au, G. Maker@murdoch edu, and Garth Lucas Maker. "Regulation of surfactant production by fetal type II pneumocytes and the characterization of fibroblast-pneumocyte factor." Murdoch University, 2008. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20080430.141113.

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The fetal lung undergoes extensive physiological and biochemical maturation prior to birth in preparation for its postnatal function as an organ for gas exchange. Pulmonary surfactant, a substance that reduces surface tension and prevents alveolar collapse, is produced by type II pneumocytes within the lung. Reduced ability to produce surfactant leads to neonatal respiratory distress syndrome. Synthesis of the phospholipid component of surfactant, phosphatidylcholine (PC), is stimulated by fibroblast-pneumocyte factor (FPF), a protein expressed by fibroblast cells within the fetal lung. Although its function is well known, the identity of this important protein has remained a mystery. Recent research has suggested that FPF may be neuregulin-1, a growth factor found in many tissues during development. Enhanced synthesis of PC (and therefore detection of FPF) is measured using a tissue culture-based method. Primary cultures of lung fibroblasts and type II pneumocytes are prepared, and fibroblast-conditioned medium (FCM) is exposed to the type II cells. Resultant PC synthesis is measured using radioisotope-labeled PC-precursor and a chloroform-based lipid extraction method. Initial results using this method were very inconsistent, so a study was undertaken to determine which parts of the method could be contributing to this inconsistency. Cell density of type II cultures (measured in μg DNA.plate-1) was shown to have a significant effect on results. Treatment of fibroblasts with 100 nM dexamethasone and exposure of type II cultures to the resultant FCM caused a mean 9.17% increase in PC synthesis, but when only type II cultures with a cell density below 25 μg DNA.plate-1 were analyzed, this value increased to 17.56%. Type II cultures with cell density above this threshold value showed a mean increase in synthesis of only 3.39%. The consistent application of [3H]-choline chloride also had a significant effect on results. Experiments utilizing phorbol 12-myristate 13-acetate to stimulate fibroblasts were very inconsistent. The mean activity of the initial [3H]-choline chloride solution prepared for these experiments was found to be 2.04 μCi.mL-1, compared to a mean of 4.79 μCi.mL-1 for all other experiments. Observations from this section of the study led to considerable revision of the method used to measure PC synthesis. Quadrupolar ion trap mass spectrometry (MS) was used to analyze FCM and determine if neuregulin-1 (NRG1) could be FPF. A mass spectrum was obtained for recombinant NRG1, with predominant ions of 1068, 1142 and 1246 m/z. All three of these ions were also detected in both control and dexamethasone-treated FCM. Partial fragmentation of 1068 m/z of NRG1 was achieved using MS2, and generated a base peak of 1047 m/z. This fragmentation was also observed in 1068 m/z from FCM. LC/MS was utilized to quantify NRG1 in FCM, using a standard curve generated using recombinant NRG1. Control FCM had a NRG1 concentration of 19.85 μg.mL-1, while the concentration in dexamethasone treated FCM was 41.59 μg.mL-1. FCM which had given no positive response to dexamethasone when tested using the indirect cultured cell system had a control NRG1 concentration of 20.85 μg.mL-1, and a dexamethasone treated concentration of 22.84 μg.mL-1. These values were not significantly different from the control value for FCM in those fibroblast cultures that had generated a positive response to dexamethasone. Results of this section of the study have provided strong evidence that NRG1 is a major component of FPF, and a review of the NRG1 signaling pathway further supports this conclusion. Insulin-like growth factors (IGFs) are functionally related to neuregulins and are known to be important in fetal development. The effect of IGF-II on synthesis of surfactant PC and its subsequent secretion from type II pneumocytes was studied. In terms of PC synthesis, IGF-II was tested at concentrations of 0.4, 0.6 and 0.8 μM. The mean increase in synthesis was found to be 6.00, 6.15 and 6.91%, respectively. These values were not significantly different from control values. Secretion of PC was tested over the concentration range of 0.1 to 1.6 μM, with no significant effect observed. Possible inhibition by IGF-II was also studied, using the known stimulants of secretion, neuromedin C and isoproterenol. No significant effect on the enhanced level of secretion was observed when IGF-II was added with either secretagogue. Lack of an appropriate receptor and/or the possibility that cultured cells may not exactly mimic the situation in vivo are probably the reasons IGF-II has no effect on either synthesis or secretion.
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Maker, Garth Lucas. "Regulation of surfactant production by fetal type II pneumocytes and the characterization of fibroblast-pneumocyte factor." Maker, Garth Lucas (2008) Regulation of surfactant production by fetal type II pneumocytes and the characterization of fibroblast-pneumocyte factor. PhD thesis, Murdoch University, 2008. http://researchrepository.murdoch.edu.au/486/.

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The fetal lung undergoes extensive physiological and biochemical maturation prior to birth in preparation for its postnatal function as an organ for gas exchange. Pulmonary surfactant, a substance that reduces surface tension and prevents alveolar collapse, is produced by type II pneumocytes within the lung. Reduced ability to produce surfactant leads to neonatal respiratory distress syndrome. Synthesis of the phospholipid component of surfactant, phosphatidylcholine (PC), is stimulated by fibroblast-pneumocyte factor (FPF), a protein expressed by fibroblast cells within the fetal lung. Although its function is well known, the identity of this important protein has remained a mystery. Recent research has suggested that FPF may be neuregulin-1, a growth factor found in many tissues during development. Enhanced synthesis of PC (and therefore detection of FPF) is measured using a tissue culture-based method. Primary cultures of lung fibroblasts and type II pneumocytes are prepared, and fibroblast-conditioned medium (FCM) is exposed to the type II cells. Resultant PC synthesis is measured using radioisotope-labeled PC-precursor and a chloroform-based lipid extraction method. Initial results using this method were very inconsistent, so a study was undertaken to determine which parts of the method could be contributing to this inconsistency. Cell density of type II cultures (measured in mcg DNA.plate-1) was shown to have a significant effect on results. Treatment of fibroblasts with 100 nM dexamethasone and exposure of type II cultures to the resultant FCM caused a mean 9.17% increase in PC synthesis, but when only type II cultures with a cell density below 25 mcg DNA.plate-1 were analyzed, this value increased to 17.56%. Type II cultures with cell density above this threshold value showed a mean increase in synthesis of only 3.39%. The consistent application of [3H]-choline chloride also had a significant effect on results. Experiments utilizing phorbol 12-myristate 13-acetate to stimulate fibroblasts were very inconsistent. The mean activity of the initial [3H]-choline chloride solution prepared for these experiments was found to be 2.04 mcg Ci.mL-1, compared to a mean of 4.79 mcgCi.mL-1 for all other experiments. Observations from this section of the study led to considerable revision of the method used to measure PC synthesis. Quadrupolar ion trap mass spectrometry (MS) was used to analyze FCM and determine if neuregulin-1 (NRG1) could be FPF. A mass spectrum was obtained for recombinant NRG1, with predominant ions of 1068, 1142 and 1246 m/z. All three of these ions were also detected in both control and dexamethasone-treated FCM. Partial fragmentation of 1068 m/z of NRG1 was achieved using MS2, and generated a base peak of 1047 m/z. This fragmentation was also observed in 1068 m/z from FCM. LC/MS was utilized to quantify NRG1 in FCM, using a standard curve generated using recombinant NRG1. Control FCM had a NRG1 concentration of 19.85 mcg.mL-1, while the concentration in dexamethasone treated FCM was 41.59 mcg.mL-1. FCM which had given no positive response to dexamethasone when tested using the indirect cultured cell system had a control NRG1 concentration of 20.85 mcg.mL-1, and a dexamethasone treated concentration of 22.84 mcg.mL-1. These values were not significantly different from the control value for FCM in those fibroblast cultures that had generated a positive response to dexamethasone. Results of this section of the study have provided strong evidence that NRG1 is a major component of FPF, and a review of the NRG1 signaling pathway further supports this conclusion. Insulin-like growth factors (IGFs) are functionally related to neuregulins and are known to be important in fetal development. The effect of IGF-II on synthesis of surfactant PC and its subsequent secretion from type II pneumocytes was studied. In terms of PC synthesis, IGF-II was tested at concentrations of 0.4, 0.6 and 0.8 mcM. The mean increase in synthesis was found to be 6.00, 6.15 and 6.91%, respectively. These values were not significantly different from control values. Secretion of PC was tested over the concentration range of 0.1 to 1.6 mcgM, with no significant effect observed. Possible inhibition by IGF-II was also studied, using the known stimulants of secretion, neuromedin C and isoproterenol. No significant effect on the enhanced level of secretion was observed when IGF-II was added with either secretagogue. Lack of an appropriate receptor and/or the possibility that cultured cells may not exactly mimic the situation in vivo are probably the reasons IGF-II has no effect on either synthesis or secretion.
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Delbrel, Eva. "Implication de l'hypoxie et du stress du réticulum endoplasmique dans l'altération phénotypique des cellules épithéliales alvéolaires." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCD081.

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La fibrose pulmonaire idiopathique (FPI) est une maladie rare, au pronostic sombre, pour laquelle il n’existe aucun traitement curatif. Elle se caractérise par un remodelage du poumon distal, avec le remplacement progressif mais irréversible du parenchyme alvéolaire en un tissu fibreux. L’épithélium alvéolaire, soumis à de nombreuses micro-agressions (polluants, virus…) assure un processus de ré-épithélialisation non contrôlé. Cette perturbation est associée à une dysfonction des cellules progénitrices de l’épithélium, les cellules épithéliales alvéolaires (CEAs) de type II ou pneumocytes de type II (PII). Chez les patients atteints de FPI, l’activation des voies hypoxiques est attestée par l’expression du facteur de transcription hypoxia-inducible factor 1 (HIF-1). Par ailleurs, la présence d’un stress du RE est observé par l’activation des voies de l’unfolded protein pathway (UPR) ainsi que par l’expression de CHOP. La première partie des travaux de thèse caractérise la réponse des CEAs à l’hypoxie aigue in vivo dans un modèle de rat et in vitro dans des CEAs de rat. L’apoptose a été évaluée et l’implication des acteurs de l’UPR dans l’activation des voies apoptotiques en hypoxie a été mise en évidence. Le contrôle de HIF-1 dans l’induction des voies de l’UPR a également été démontré. Dans une seconde partie, le rôle des voies de l’UPR dans l’acquisition de caractéristiques mésenchymateuses a été décrit. Les mécanismes moléculaires impliqués dans cette régulation ont été caractérisés. Ces travaux mettent en exergue le rôle primordial des voies de l’UPR dans l’altération phénotypique des CEAs en hypoxie et suggèrent HIF/UPR comme un axe majeur de la pathogenèse de la FPI<br>Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and deadly lung disease characterized by a usual interstitial pneumonia (UIP) pattern associating fibrotic remodeling. This fibrotic process is related to repeated micro-injuries on alveolar epithelium leading to alveolar epithelial cells (AECs) dysfunction. The majors well-defined events in the pathogenic process in IPF are AECs apoptosis and EMT, orchestrating a progressive loss of epithelial phenotype IPF. These phenomena play a critical in the dysregulated cross-talk with subjacent interstitial fibroblasts conducting in their activation and resulting in an excessive and irreversible extracellular matrix production.In lung biopsy of pulmonary fibrosis, hypoxic microenvironment has been reported by the use of pimonidazole probe but also through expression of hypoxia inducible factor 1 (HIF-1).Another cellular event, the ER stress activation, has been described by the induction of the unfolded protein response (UPR) transcription factors ATF4 and ATF6N. Moreover, the proapoptotic transcription factor CHOP, a common target of these UPR actors, is also observed in AECs of patients.In our work, we study the connection between hypoxic and UPR pathways and its specific role in the process of AECs alteration. We characterized in vivo in an hypoxic rat lung model, in vitro in primary rat AECs exposed to hypoxia and ex vivo in lung biopsy, the molecular mechanism involved in ER stress induction. We demonstrated the implication of the UPR pathways in the hypoxic induction of apoptosis. In this context, we demonstrated the major role of HIF-1 in the control of UPR actor’s expression and in CHOP regulation. Moreover, we evaluated the involvement of UPR pathways in the induction of EMT feature in hypoxia. Molecular mechanisms involved in these regulation has been characterized. Our work highlight the cutting role of UPR pathways in AECs phenotype alteration in hypoxic microenvironment and point out HIF-1/UPR as a new major axis in IPF pathogenesis
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Witherden, Ian Richard. "Investigation of mechanisms of pulmonary inflammation utilizing a pneumocyte in vitro model." Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272028.

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Kemp, Paul J. "Ion and solute transport in alveolar type II pneumocytes." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.253135.

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Uzunhan, Yurdagül. "Effet des cellules souches mésenchymateuses dans les altérations épithéliales alvéolaires induites par l'hypoxie." Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCD103/document.

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La fibrose pulmonaire idiopathique (FPI) et le syndrome de détresse respiratoire aiguë (SDRA) de l’adulte constituent des affections sévères et létales du poumon profond associées à une hypoxie alvéolaire, pour lesquelles les ressources thérapeutiques sont limitées. La thérapie cellulaire utilisant des cellules souches mésenchymateuses humaines (CSMh) est actuellement envisagée dans ces pathologies, mais les mécanismes d’action des CSMh restent à élucider. Nous avons testé in vitro l’hypothèse selon laquelle les CSMh pourraient exercer un effet cytoprotecteur paracrine sur les cellules épithéliales alvéolaires (CEA) soumises à l’hypoxie.Dans une première étude, nous avons montré que l’exposition aiguë de CSMh dérivées de moelle osseuse à un environnement inflammatoire (traitement par cytomix constitué de TNFα, d’Interféron Ƴ et d’Interleukine 1β) et hypoxique (3% O₂) mimant le microenvironnement alvéolaire du SDRA ne modifiait pas le phénotype ou la viabilité des cellules mais induisait des modifications de leur secretome, notamment de facteurs connus pour réguler le transport trans-épithélial alvéolaire de sodium (Na) et la réabsorption de l’oedème alvéolaire : IL1-ra, PGE2 et KGF. Le milieu de culture des CSMh (MC-CSMh), qu’il soit obtenu en normoxie ou en hypoxie-cytomix, prévenait l’augmentation de la perméabilité épithéliale des CEA primaires de rat cultivées sur support semi-perméable et exposées à l’hypoxie et au cytomix. Le MC-CSMh provenant de CSMh cultivées en normoxie prévenait l’inhibition du transport transépithélial alvéolaire de Na en restaurant l’expression à la surface de la sous-unité α du canal sodique épithélial ENaC, tandis que le MC-CSMh obtenu sous hypoxie-cytomix n’avait pas d’effet protecteur. La sécrétion de Keratinocyte Growth Factor (KGF) par les CSMh était indispensable à leur effet protecteur.Dans une seconde étude, nous avons montré qu’une exposition prolongée à l’hypoxie telle que rencontrée au cours de la FPI induisait des modifications phénotypiques des CEA de rat évocatrices de transition épithélio-mésenchymateuse (TEM) avec perte progressive d’expression des marqueurs épithéliaux (TTF1, AQP5, ZO-1 et E-Cadhérine) couplée à l’apparition tardive de marqueurs mésenchymateux (α -SMA et Vimentine). Ces modifications phénotypiques s’accompagnaient de l’expression à la phase initiale de l’hypoxie de facteurs de transcription impliqués dans la TEM (SNAI1, TWIST1 et ZEB1) ou induits par l’hypoxie (HIF-1α et HIF-2α et de protéines induisant la TEM (TGFβ1 et CTGF). La co-culture des CEA avec des CSMh en fond de puits prévenait les modifications phénotypiques induites par l’hypoxie ainsi que l’expression des facteurs pro-TEM TWIST1, ZEB1, TGFβ1 et CTGF. Là encore, le KGF était au moins en partie responsable des effets protecteurs des CSMh.Ces deux études indiquent que les CSMh sont susceptibles d’exercer des effets cytoprotecteurs paracrines vis-à-vis des CEA soumises à l’hypoxie aiguë ou prolongée, en limitant d’une part les effets de délétères de l’hypoxie sur les propriétés de transport vectoriel de Na et en prévenant d’autre part les modifications phénotypiques évocatrices de TEM. La sécrétion par les CSMh de KGF, facteur de croissance épithélial bien connu pour ses effets bénéfiques sur les CEA, explique en partie les effets protecteurs paracrines des CSMh. Nos résultats suggèrent que les effets cytoprotecteurs des CSMh vis-à-vis des CEA pourraient contribuer aux effets bénéfiques des CSMh observés in vivo dans différents modèles animaux d’agressions alvéolaires aiguës ou à tendance fibrosante<br>Non communiqué
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Fois, Georgio [Verfasser]. "Response of alveolar type II pneumocytes to mechanical stimulation / Giorgio Fois." Ulm : Universität Ulm. Medizinische Fakultät, 2012. http://d-nb.info/1019167831/34.

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Lesur, Olivier. "Influence des poussières minérales et des liquides de lavage bronchoalvéolaire de silicone sur l'activité du pneumocyte II in vitro." Nancy 1, 1992. http://www.theses.fr/1992NAN10027.

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La caractérisation morphologique et biochimique d'une population purifiée de pneumocytes II ftaux de rats a permis une étude de son comportement devant l'exposition à deux intervenants majeurs de la silicose: les poussières minérales et les liquides de lavages bronchoalvéolaires. La silice, par ses propriétés de surface, est toxique aux doses élevées et mitogène aux faibles doses. Les liquides alvéolaires humains et ovins exposes in vivo a la silice sont nettement mitogènes par rapport à ceux non exposes. L'activité proliférative est corrélée à la cellular ite alvéolaire concomitante et semble en partie due à des molécules de type pdgf- et fgf-acide like. La silice n'a pas d'activité directe sur le métabolisme phospholipidique du pneumocyte II, tandis que les liquides alvéolaires stimulent l'activité de synthèse de novo des phospholipides et en inhibent la sécrétion. Ces altérations sont exacerbées dans la silicose et impliqueraient au moins en partie l'apoprotéine a du surfactant, retrouvée en grande quantité dans les liquides alvéolaires de silicose ovine. L'activité de réduction de tension de surface des composants du surfactant ovin est néanmoins observée dans la silicose
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Molliex, Serge. "Effets de l'halothane sur les pneumocytes II de rat en culture primaire." Saint-Etienne, 1991. http://www.theses.fr/1991STET6417.

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Books on the topic "Pneumocyty"

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Lofthouse, Andrea Kay. Investigation of the lectin histochemistry of human type II pneumocytes, human bronchial seromucinous glands and human salivary glands. University of Manchester, 1993.

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Book chapters on the topic "Pneumocyty"

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Schiller, Erich. "Pneumocytes." In Free Radicals and Inhalation Pathology. Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18619-6_8.

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Kerr, Keith M., and Andras Khoor. "Multifocal Micronodular Pneumocyte Hyperplasia." In Encyclopedia of Pathology. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-69263-0_4343.

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Kerr, Keith M., and Andras Khoor. "Multifocal Micronodular Pneumocyte Hyperplasia." In Encyclopedia of Pathology. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-28845-1_4343-1.

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Maina, J. N. "Pneumocytes, Surfactant and Design of Gas Exchangers." In Advances in Anatomy Embryology and Cell Biology. Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-55917-4_13.

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Banks, Melanie A., Dale W. Porter, William G. Martin, and Vincent Castranova. "Taurine Protects Against Oxidant Injury to Rat Alveolar Pneumocytes." In Advances in Experimental Medicine and Biology. Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3436-5_40.

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Haller, Thomas, and Paul Dietl. "Imaging the Stages of Exocytosis in Epithelial Type II Pneumocytes." In Neuromethods. Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-676-4_2.

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Oda, Y., H. Kai, K. Takaki, et al. "Pulmonary Surfactant Secretion in the Type II Pneumocytes in Inflamed Condition." In Mediators in Airway Hyperreactivity. Birkhäuser Basel, 1990. http://dx.doi.org/10.1007/978-3-0348-7379-6_17.

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Taylor, Steve, and Steven Meshnick. "Pneumocysti." In Molecular Detection of Human Fungal Pathogens. CRC Press, 2011. http://dx.doi.org/10.1201/b11375-74.

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"Cranial Pneumocyst." In Encyclopedia of Clinical Neuropsychology. Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_3382.

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Marin, Léa. "The Type II Pneumocyte." In Pulmonary Surfactant: Biochemical, Functional, Regulatory, and Clinical Concepts. CRC Press, 2019. http://dx.doi.org/10.1201/9780367812812-2.

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Conference papers on the topic "Pneumocyty"

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Mak, Garbo, and Marcia Katz. "Multifocal Multinodular Pneumocyte Hyperplasia In Tuberous Sclerosis." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3844.

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Mahan, Anne, Yao Chen, and Margaret A. Schwarz. "Alpha5Beta1 Integrin / Fibronectin Interactions Mediate Type 2 Pneumocyte Adhesion." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1853.

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Chamoto, Kenji, Barry C. Gibney, Maximilian Ackermann, et al. "Regulation Of Post-Pneumonectomy Angiogenesis By Type II Pneumocytes." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6854.

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van Batenburg, Aernoud, Reinier Snetselaar, Roel Goldschmeding, Jan Grutters, Karin Kazemier, and Coline van Moorsel. "Telomere shortening in type II pneumocytes relates to idiopathic pulmonary fibrosis." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa1825.

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Chung, Eun Joo, Luca F. Valle, Ayla O. White, and Deborah E. Citrin. "Abstract 3049: Arachidonate 12-lipoxygenase contributes to radiation-induced type II pneumocyte senescence and fibrosis." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3049.

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Desseigne, Marine, Virginie Avrillon, Anne Lise Bienvenu, et al. "Risk factors of pneumocytis pneumoniae in solid tumours: A case-control study." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa576.

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Song, Changcheng, Thomas J. Rogers, Friedrich Kueppers, and Steven G. Kelsen. "Cigarette Smoke (CS) Condensate Induces The Aggregation Of Alpha-1 Antitrypsin (AAT) In Pneumocytes." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2644.

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Simpson, E., A. D. Rice, T. Wang, and M. B. Fallon. "The Role of Placental Growth Factor as a Mediator of Pulmonary Disease Via Human Alveolar Type 2 Pneumocyte Apoptosis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2129.

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TELES, Lucas Pinheiro Machado, Mariana Aragão PASSOS, and Marcos Alves PAVIONE. "RELATO DE USO EXPERIMENTAL DE CATETER PNEUMOCATH PARA DRENAGEM DE PNEUMOTÓRAX EM UM LACTENTE EM UTI PEDIÁTRICA PÚBLICA DE SERGIPE." In Anais do II congresso de urgência e emergência de Sergipe: os desafios na assistência multiprofissional em emergências. Even3, 2018. http://dx.doi.org/10.29327/15103.2-2.

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Nachman, R. L., R. L. Silverstein, and A. S. Asch. "THROMBOSPONDIN: CELL BIOLOGY OF AN ADHESIVE GLYCOPROTEIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644653.

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Thrombospondin (TSP), a multifunctional 450 KD glycoprotein is a secretory product of thrombin stimulated platelets. It is a major component of the platelets alpha granule constituting approximately 3% of total platelet protein. Thrombospondin does not circulate in appreciable concentrations ∽0 100 ng/ml); however, the tissue distribution is broad. In addition to its expression on the membrane of activated platelets, the protein is synthesized by fibroblasts endothelial cells, glial cell smooth muscle cells alveolar pneumocytes mononuclear phagocytes and various tumor cells. TSP is a major constituent of the extracellular matrix and has been demonstrated in the vessel wall, basement membrane and glandular connective tissue. Fibroblasts, smooth muscle cells and endothelial cells in tissue culture incorporate TSP into the extracellular matrix. Matrix TSP is under cell-cycle regulatory control. Mesenchymal cells in the proliferative phase synthesize greater amounts of TSP than non growing cells. Platelet derived growth factor induces smooth muscle cell and glial cell synthesis of TSP. Atheromatous lesions contain increased amounts of TSP compared to normal vessels emphasizing the potential role of TSP in the interaction of proliferating cells with the matrix. TSP binds specifically, saturably, and reversibly to mouse peritoneal macrophages and to cells of the monocyte-like human cell line U937. Binding was time dependent and was optimal in the presence of both Ca++ and Mg++. PMA stimulated U937 cells and activated macrophages bound TSP to an equivalent extent as resting cells. The TSP binding site on the surface of U937 cells and peripheral blood monocytes mediates the adhesive interaction between these cells and thrombin-stimulated platelets. Using a sensitive rosetting assay we found that monocytes were not rosetted by resting platelets while &gt;90% were rosetted by thrombin-stimulated platelets. Monoclonal and polyclonal anti-TSP antibodies markedly inhibited rosetting as did TSP itself. Antifibronectin or non-immune control antibodies did not inhibit rosetting, nor did fibronectin, fibrinogen, the fibronectinadhesion tetrapeptide arg-gly-asp-ser (RGDS), or heparin. The TSP membrane receptor, an 88 KD glycoprotein, formely known as GPIV has been identified in platelets, endothelial cells, monocytes and a variety of tumor cells. TSP may thus serve as a molecular bridge linking activated platelets with monocytes at sites of early vascular injury. Such interactions involving the TSP receptor complex may be of critical importance in the regulation of thrombosis and the initiation of atherosclerosis.
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