Дисертації з теми "Alveolar type cell"
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Bhandari, R. N. B. "Characterization of a cell adhesion receptor on rat lung alveolar type 2 cells." Thesis, Imperial College London, 1988. http://hdl.handle.net/10044/1/46962.
Повний текст джерелаHofer, Christian Carlisle. "Effects of Influenza Infection on Murine Alveolar Type II Cell Function." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1406201295.
Повний текст джерелаHasegawa, Kouichi. "Fraction of MHCII and EpCAM expression characterizes distal lung epithelial cells for alveolar type 2 cell isolation." Kyoto University, 2018. http://hdl.handle.net/2433/232118.
Повний текст джерелаDowns, Charles. "Cigarette Smoke Extract-Induced Injury in Alveolar Cells in Model Systems." Diss., The University of Arizona, 2011. http://hdl.handle.net/10150/201510.
Повний текст джерелаDowns, Charles A., Abdel A. Alli, Nicholle M. Johnson, and My N. Helms. "Cigarette smoke extract is a Nox agonist and regulates ENaC in alveolar type 2 cells." AMER INST MATHEMATICAL SCIENCES-AIMS, 2016. http://hdl.handle.net/10150/621494.
Повний текст джерелаClegg, Gareth Roger. "Co-expression of lung alveolar epithelial type I and II cell-selective proteins in response to injury." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/29066.
Повний текст джерелаKorogi, Yohei. "In Vitro Disease Modeling of Hermansky-Pudlak Syndrome Type 2 Using Human Induced Pluripotent Stem Cell-Derived Alveolar Organoids." Kyoto University, 2019. http://hdl.handle.net/2433/243303.
Повний текст джерелаDysart, Marilyn Markowski. "Remodeling of the pulmonary microenvironment controls transforming growth factor-beta activation and alveolar type II epithelial to mesenchymal transition." Diss., Georgia Institute of Technology, 2014. http://hdl.handle.net/1853/53421.
Повний текст джерелаDoolittle, Lauren May. "The Impact of Alveolar Type II Cell Mitochondrial Damage and Altered Energy Production on Acute Respiratory Distress Syndrome Development During Influenza A Virus Infection." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu159224389333959.
Повний текст джерелаAssis, Adriano Freitas de. "Desenvolvimento do fenótipo osteoblástico em células derivadas de osso alveolar humano cultivadas sobre titânio revestido com colágeno tipo I." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/58/58136/tde-30062008-140042/.
Повний текст джерелаCellular and extracellular events that occur during titanium (Ti) osseointegration process are highly influenced by its surface properties, such as morphology, topography and chemical composition. The objective of biochemical modification of Ti is to immobilize proteins or peptides on its surface in order to induce specific cellular and tissue responses at the boneimplant interface in order to accelerate or enhance osseointegration. The aim of this study was to evaluate the osteoblastic phenotype development in cells grown on collagen type I-coated Ti surface. Osteoblastic cells from human alveolar bone fragments were cultured on turned Ti either coated with collagen type I (col-Ti) or not (turned-Ti) and the following parameters were assessed: cell adhesion, morphology, and proliferation, total protein content, alkaline phosphatase (ALP) activity, bone-like formation and gene expression of osteoblastic markers by real-time polymerase chain reaction (real-time PCR). Col-Ti altered culture growth and gene expression of osteoblastic markers without affecting cell adhesion, morphology, protein synthesis, ALP activity, and matrix mineralization. These results demonstrated that col-Ti favours cell growth during the proliferative phase and osteoblastic differentiation, as demonstrated by changes in mRNA expression profile during the matrix mineralization phase, suggesting that this Ti surface modification may affect the processes of bone healing and remodelling.
Sitaraman, Sneha. "Alveolar type 2 epithelial cells in lung development and disease." University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1571062200291287.
Повний текст джерелаRako, Zvonimir A. [Verfasser]. "miRNA-154 mediates the transdifferentiation of alveolar type II to alveolar type I cells in the mouse model of Bronchopulmonary Dysplasia / Zvonimir Andelko Rako." Gießen : Universitätsbibliothek, 2020. http://d-nb.info/1219983101/34.
Повний текст джерелаRako, Zvonimir Andelko [Verfasser]. "miRNA-154 mediates the transdifferentiation of alveolar type II to alveolar type I cells in the mouse model of Bronchopulmonary Dysplasia / Zvonimir Andelko Rako." Gießen : Universitätsbibliothek, 2020. http://d-nb.info/1219983101/34.
Повний текст джерелаCherlet, Tracy C. "Tetrahydrocannabinol and lung surfactant metabolism in isolated fetal type II alveolar cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0025/MQ51693.pdf.
Повний текст джерелаKanj, Rania S. "Interaction between primary alveolar macrophages and primary alveolar type II cells under basal conditions and after lipopolysaccharide or quartz exposure." Morgantown, W. Va. : [West Virginia University Libraries], 2004. https://etd.wvu.edu/etd/controller.jsp?moduleName=documentdata&jsp%5FetdId=34.
Повний текст джерелаTitle from document title page. Document formatted into pages; contains x, 130 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 120-130).
Yu, Ching-lam, and 余靜霖. "Influenza H5N1 and H1N1 virus infection and innate immune responses inhuman alveolar type I, type II epithelial cells and macrophages." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B4552807X.
Повний текст джерелаSammohi, Shamili. "Effect of progesterone, terbutaline and leptin on the function of alveolar type II cells." Wright State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=wright1441040764.
Повний текст джерелаGereke, Marcus [Verfasser]. "Crosstalk between autoreactive T cells and alveolar type II epithelial cells in inflammation and tolerance / Marcus Gereke." Braunschweig : Universitätsbibliothek der Technischen Universität Braunschweig, 2017. http://d-nb.info/1127355147/34.
Повний текст джерелаGarrison, Derek S. "Rationale for the Study of Fatty Acid Binding Protein 5 in Alveolar Type II Cells." University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1226862267.
Повний текст джерелаSinger, Katharina Julia [Verfasser], and Susanne [Akademischer Betreuer] Krauss-Etschmann. "MicroRNA profiling of purified alveolar epithelial type II cells from normal mice / Katharina Julia Singer ; Betreuer: Susanne Krauss-Etschmann." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1190563401/34.
Повний текст джерелаSamuels, Emile Rasheed. "Calcium²§+-PS-dependent protein kinase C activity in fetal, neonate and adult rabbit lung and the release of surfactant-related material from isolated fetal rabbit type II alveolar cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq23487.pdf.
Повний текст джерелаMarten, Elger [Verfasser], and Christiane [Akademischer Betreuer] Dammann. "Interdependent TTF1 - ErbB4 interactions are critical for surfactant protein-B homeostasis in primary mouse lung alveolar type II cells / Elger Marten ; Akademischer Betreuer: Christiane Dammann ; Zentrum Kinderheilkunde und Jugendmedizin Abteilung Pädiatrische Pneumologie und Neonatologie der Medizinischen Hochschule Hannover." Hannover : Bibliothek der Medizinischen Hochschule Hannover, 2016. http://d-nb.info/1108556582/34.
Повний текст джерелаJacob, Anjali. "Generation of mature type II alveolar epithelial cells from human pluripotent stem cells." Thesis, 2017. https://hdl.handle.net/2144/26476.
Повний текст джерелаLo, Bernice. "Regulation of Adaptive Immunity in the Lung by the Alveolar Epithelial Type II Cell and Surfactant Protein a." Diss., 2008. http://hdl.handle.net/10161/711.
Повний текст джерелаDue to its nature and function, the lungs are confronted with the unique challenge of rapidly eliminating inhaled pathogens and particulates while limiting inflammatory responses. A disruption in this immune homeostasis may result in respiratory inflammatory diseases, such as allergies or asthma. The alveolar epithelial type II cell and its secretory product, surfactant protein A (SP-A), have been linked to roles in adaptive immunity in the lung. The discovery that type II cells constitutively express major histocompatibility complex class II (MHC II) suggested that type II cells may function to present antigen to T cells. Studies in vitro demonstrated that SP-A inhibits the maturation of bone marrow-derived dendritic cells. The goal of this work was to determine how type II cells and SP-A may be functioning to regulate adaptive immunity in the lungs. The hypothesis tested is that type II cells and SP-A suppress the activity of T cells and dendritic cells in the lungs. As T cells and dendritic cells are critical for the initiation and function of the adaptive immune response, the inhibition of T cell and dendritic cell activity would limit inflammation in the lungs. Although isolated murine type II cells expressed MHC II, they did not express detectable levels of the costimulatory molecules CD80 and CD86 and were poor activators of T cells. Upregulation of MHC II on type II cells by interferon-gamma stimulation did not enhance the ability of type II cells to activate T cells. Instead, the type II cells suppressed T cells from subsequent activation to antigen in an antigen-dependent manner, indicative of tolerance. T cells pre-incubated with type II cells and antigen were suppressed from further activation, even after removal of the type II cells. Using a model of pulmonary infection with Mycoplasma pneumoniae, wildtype mice were found to have fewer mature dendritic cells in the mediastinal lymph nodes than SP-A null mice. The presence of SP-A in the wild-type mice had a suppressive effect on the M. pneumoniae-induced maturation of dendritic cells in the lungs. Together, the data demonstrate that type II cells and SP-A participate in the adaptive immune response by suppressing the activity of T cells and dendritic cells in the lungs.
Dissertation
Sun, Yuliang Leon. "The role of ATP binding cassette A3 (ABCA3) in health and disease using pluripotent stem cell-derived type II alveolar epithelial cells." Thesis, 2020. https://hdl.handle.net/2144/41103.
Повний текст джерела2021-05-26T00:00:00Z
CHEN, SHIUAN-TING, and 陳萱廷. "Continuous hypoxia and intermittent hypoxia-reoxygenation affect the expression of hypoxia-inducible factors, stem cell markers, type II alveolar cell marker SPC, and NOTCH and WNT signaling genes in human small airway epithelial cells (SAEC)." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/5tm7pb.
Повний текст джерела國防醫學院
航太及海底醫學研究所
107
Previous studies have shown that chronic long-term hypoxia and hypoxic-reoxygenation (H/R), which mimics ischemia-reperfusion, both regulate inflammatory responses in mammalian airway epithelial cells and induce oxidative stress and injury, including increased production of reactive oxygen species (ROS) and reduced production of ATP and alveolar surfactant proteins. However, it has not been reported whether hypoxia and H/R regulate proliferation, differentiation, apoptosis, and expression of hypoxia-inducible factors, alveolar type II cell markers, stem/progenitor cell markers as well as WNT and NOTCH signaling factors in airway epithelial cells, and whether hypoxia and H/R exert different effects on gene/protein expression in healthy (normal) versus diseased airway epithelial cells. We found that both hypoxia and H/R significantly reduced expression of hypoxia-inducible factor HIF1A, lung precursor/stem cell marker gene, type II alveolar epithelial cell marker protein SPC, and NOTCH3 signaling gene in both N-SAECs and D-SAECs. H/R decreased NOTCH1 expression in N-SAECs, contrary to the increased NOTCH1 expression in D-SAECs. On the other hand, the expression levels of HIF2A, TP63, HEY1, WNT5A, FZD4, CDK1, MKI67 and TP53AIP1 are differentially regulated by hypoxia and H/R in N-SAECs and D-SAECs. The aforementioned changes of gene/protein expression under VII hypoxia and H/R are applicable as reference criteria for future lung organoid culture in vitro and clinical transplantation in vivo.
Merluza, John. "Nicotine and cotinine effects on fetal rat lung type II alveolar cells." 2006. http://hdl.handle.net/1993/20898.
Повний текст джерелаLin, Bo-Shen, and 林伯軒. "Identification and characterization of a lysophosphatidylcholine acyltransferase in alveolar type II cells." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/84449967655915403380.
Повний текст джерела輔仁大學
基礎醫學研究所碩士班
95
The alveolus is the major gas exchange unit in lungs. The alveolar epithelium is mainly composed of two types of cells, alveolar type I and type II cells. The major function of type II cells is to produce pulmonary surfactant. Pulmonary surfactant is secreted from alveolar type II cells to the air–liquid interface where it reduces surface tension and prevents atelectasis of alveoli. Pulmonary surfactant is composed of phospholipids and surfactant proteins. Phospholipids include phosphatidylcholines (PC), mainly dipalmitoylphosphatidylcholine (DPPC), and phosphatidylglycerols. DPPC is most responsible for the surface tension-lowering properties of pulmonary surfactant. Production of DPPC can be achieved by both de novo synthesis and the remodeling pathways. In the remodeling pathway, unsaturated acyl group of cellular phosphatidylcholines is removed by phospholipase A2 resulting in 1-palmitoyl-2- lysophosphatidylcholines, followed by reacylation of 1-palmitoyl-2-lysophos- phatidylcholines with palmitoyl-CoA via the catalysis of a lysophosphatidylcholine (lysoPC) acyltransferase (LPCAT). We identified a putative LPCAT whose expression is enriched in alveolar type II cells of Sprague Dawley (SD) rat. The cloned cDNA encodes a protein of 534 amino acids with an estimated molecular mass of 59 kDa. Amino acid sequences of this putative acyltransferase revealed a highly conserved domain similar to 1-acyl-sn-glycerol-3-phosphate acyltransferase (plsC) in Escherichia coli(E. coli). Using prokaryotic expression system, a maltose binding protein and 6x histidine tagged LPCAT was successfully expressed and purified using affinity chromatography. Purified proteins were injected into rabbits for specific anti-sera production. Anti-LPCAT antibodies were also purified from immunized sera by affinity chromatography. Using purified anti-LPCAT antibodies, we localized LPCAT protein to alveolar type II cells by immunohistochemistry, immunoflurosence and Western blotting. Using zonal centrifugation, LPCAT was localized to the microsomal organelle fraction. The result was also confirmed by confocal microscopy. Using eukaryotic 293T cell expression system in combination with zonal centrifugation, the microsomal organelle fractions from transfected cells were tested for acyltransferase activity.
Chuang, Tzu-Lin, and 莊子林. "The effect of nicotine on HGF expression in alveolar type II epithelial cells." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/79640401513915993896.
Повний текст джерела國立中興大學
生物醫學研究所
94
Hepatocyte growth factor (HGF) was first purified from serum of hepatectomized rats by Nakamura et al. in 1984, based on it’s ability to promote liver cell growth and DNA synthesis. HGF is also a potent cytokine to induce cell motility, and morphogenesis. It is mainly secreted by mesenchymal cells and acts on a wide variety of epithelial cells through binding of membrane receptor c-Met and activation on tyrosine kinase signaling cascade. The previous studies demonstrated that overexpression of HGF and c-Met often correlated with human tumorigenesis and metastasis, in particular, with the poor prognosis of cancer patients. Previously, our lab discovered that HGF mRNA was overexpressed in nontumor lung tissue of adenocarcinoma patients induced by cigarette smoke. Adenocarcinoma is a common form of lung cancer. As the increase of smoking population, cigarette smoking becomes a leading risk factor for lung cancer development, especially for lung adenocarcinoma. By in situ hybridization, we found in this study that HGF mRNA was expressed in type II alveolar epithelial cells as well as A549 cell line. In vitro, we showed that cigarette smoke derivative, nicotine, induced HGF expression in primary culture of type II cells. In vivo, we set up an animal model of mouse to evaluate cigarette smoking on HGF expression. After ten- and twenty-week cigarette smoke exposure, proliferation of type II cells increase significantly in cigarette smoking mice and HGF expression was also up-regulated. We also found that nicotine induced FAK transcription in type II cells and increased in cigarette smoking mice. According to these results, we suggest that nicotine could induce HGF expression in type II cells.
Gereke, Marcus [Verfasser]. "Crosstalk between autoreactive T cells and alveolar type II epithelial cells in inflammation and tolerance / von Marcus Gereke." 2007. http://d-nb.info/983540551/34.
Повний текст джерелаGandhi, Shephali G. "The effect of pulmonary edema fluid on ion transport by adult alveolar type II epithelial cells." 2007. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=453012&T=F.
Повний текст джерелаAhmed, Asra. "Apoptosis and caspase-3 activity in isolated fetal rat lung cells, human A549 cells and rat periodontal ligament fibroblasts following exposure to cigarette smoke extract." 2012. http://hdl.handle.net/1993/5205.
Повний текст джерелаChuang, Chi-Yuan, and 莊淇源. "STUDY OF ACUTE LUNG INJURY: MOLECULAR MECHANISMS OF LIPOPOLYSACCHARIDE-INDUCED APOPTOTIC INSULTS AND REGULATION OF surfactant protein GENE EXPRESSION IN HUMAN ALVEOLAR EPITHELIAL TYPE II CELLS." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/03097245032120426995.
Повний текст джерела臺北醫學大學
臨床醫學研究所
99
Lipopolysaccharide (LPS), a Gram-negative bacterial outer membrane component, is one of the major causes of septic shock with acute lung injury. Pulmonary alveolar epithelial type II cells have highly specialized functions for synthesizing and secreting surfactant proteins (SPs) to participate in the physiological and pathophysiological regulation of sepsis-induced acute lung injury. Alterations in the levels of surfactant components in the lungs during inflammation are quite complex. Toll-like receptors (TLRs) that play important roles in innate immunity can transduce pathogen-triggered signals to regulate certain inflammation-related gene expressions through the activation of transcription factors. In contrast to low concentration of LPS-induced physical activity, intratracheal instillation of a high concentration of LPS in mice directly caused the death of bronchial epithelial cells. Thus, LPS may have pathophysiological and toxic effects on affecting the alveolar type II epithelial cells. The purpose of this research was aimed to evaluate the molecular mechanisms of LPS-induced cell apoptosis and surfactant proteins biosynthesis using human lung carcinoma type II epithelium-like A549 cells as the experimental model. Firstly, the study was aimed to evaluate the apoptotic effect of toxic concentration of LPS in A549 cells and the possible mechanisms. Exposure of A549 cells to clinical concentration (1~10 ng/ml) of LPS did not affect cell viability, but toxic dose (1~10 μg/ml) of LPS decreased cell viability in concentration- and time-dependent manners. In parallel, LPS concentration- and time-dependently induced apoptosis of A549 cells. LPS only at a high concentration of 10 μg/ml caused mildly necrotic insults to A549 cells. Exposure of A549 cells to LPS increased the levels of cellular nitric oxide and reactive oxygen species (ROS). Pretreatment with N-acetylcysteine, an antioxidant, significantly lowered LPS-caused enhancement of intracellular ROS in A549 cells and simultaneously attenuated the apoptotic insults. Treatment of A549 cells with LPS caused significant decreases in the mitochondrial membrane potential and biosynthesis of adenosine triphosphate. LPS triggered the release of cytochrome c from the mitochondria to the cytoplasm. Activities of caspases-9 and -6 were augmented following LPS administration. Consequently, exposure of A549 cells to LPS induced DNA fragmentation in a time-dependent manner. Pretreatment of A549 cells with N-acetylcysteine significantly ameliorated LPS-caused alterations in caspase-9 activation and DNA damage. Secondly, we attempted to evaluate the signal-transducing mechanisms of LPS-caused regulation of SP-A biosynthesis in A549 cells. Exposure of A549 cells to clinical concentration (1 ng/ml) of LPS increased SP-A protein and mRNA production in concentration- and time-dependent manners without affecting SP-D mRNA production. Clinical concentration of LPS time- dependently induced TLR2 mRNA expression and increased phosphorylation of mitogen-activated protein kinase (MEK) 4 & c-Jun NH2 terminal kinase 1 (JNK1) and augmented the translocation of c-Jun from the cytoplasm to nuclei without affecting c-Fos. Application of TLR2 small interference (si)RNA into A549 cells decreased the levels of this receptor and simultaneously inhibited LPS-induced SP-A mRNA and protein syntheses. After knocking-down the translation of MyD88 by RNA interference, the LPS-triggered MEK4 phosphorylation was attenuated. Application of TLR2 siRNA decreased LPS-enhanced phosphorylation of MEK4 and JNK1. Pretreatment of A549 cells with SP600125, an inhibitor of JNK1, significantly lowered LPS-induced c-Jun translocation and SP-A mRNA production. Taken together, this study has shown that toxic concentration of LPS specifically induces apoptotic insults to human alveolar epithelial cells through ROS-mediated activation of the intrinsic mitochondrion-cytochrome c-caspase protease mechanism and clinical concentration of LPS selectively induces SP-A gene expression possibly through TLR2-mediated sequential activation of MyD88-MEK4-JNK1-AP-1 in human alveolar epithelial A549 cells The LPS-induced apoptosis and sp-a gene expression in alveolar epithelial type II cells can indicate the status of Gram-negative bacteria-caused septic shock and acute lung injury. There are certain limitations in the present study, including A549 cells are derived from human lung carcinoma. The mechanisms of LPS-induced oxidative stress, cell apoptosis and production of SPs in A549 cells may be different from normal alveolar epithelial cells. In future studies, we will perform translational study to evaluate the signal-transducing effects of LPS on alveolar epithelial cells of animals and broncho-alveolar lavages with acute lung injury to validate our in vitro data.
Samuels, Emile Rasheed. "Calcium2S+-PS-dependent protein kinase C activity in fetal, neonate and adult rabbit lung and the release of surfactant-related material from isolated fetal rabbit type II alveolar cells." 1996. http://hdl.handle.net/1993/1025.
Повний текст джерелаChupin, Cécile. "Impact du stress oxydant sur les mécanismes de clairance alvéolaire et de réparation épithéliale pulmonaires." Thèse, 2008. http://hdl.handle.net/1866/7584.
Повний текст джерела