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Dissertations / Theses on the topic 'Alveolar type cell'

Author: Grafiati

Published: 1 April 2023

Last updated: 31 July 2025

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1

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.

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2

Hofer, 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.

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3

Hasegawa, 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.

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4

Downs, Charles. "Cigarette Smoke Extract-Induced Injury in Alveolar Cells in Model Systems." Diss., The University of Arizona, 2011. http://hdl.handle.net/10150/201510.

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Cigarette smoke contributes to many diseases. The actions of second and third hand smoke, which have implications for non-smokers and the very young, are just beginning to be appreciated. The overarching hypothesis of this project is that cigarette smoke has different injurious actions on alveolar cells based on chronological age. The purpose here was to learn more about the susceptibility of alveolar cells to cigarette smoke extract (CSE)- induced injury by performing studies on pulmonary alveolar and endothelial cells derived from neonatal, young, and old rats. The aims involved: 1. Develo

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5

Downs, 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.

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There is considerable evidence that cigarette smoking is the primary etiology of chronic obstructive pulmonary disease (COPD), and that oxidative stress occurs in COPD with the family of tissue nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox) enzymes playing a significant role in lung pathogenesis. The purpose of this study was to determine the effects of cigarette smoke extract (CSE) on Nox signaling to epithelial sodium channels (ENaCs). Pre-treatment with diphenyleneiodonium (DPI), a pan-Nox inhibitor, prevented stimulatory effects of CSE on ENaC activity; open probability

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6

Clegg, 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.

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This study used a novel combination of ATI and ATII cell-selective antibodies to investigate the phenotype of the alveolar epithelium following Staphylococcus aureus-induced ‘direct’ lung injury. Following distal airway instillation of S. aureus, the alveolar epithelium was covered with ATII cells (MMC4/RTII70-positive cells) and ATI cells (RTI40-positive cells) as seen in control lungs. However, the surface area covered by ATII cells was significantly increased, while the surface area covered by ATI cells was significantly decreased, in comparison with controls. The alveolar wall of S. aure

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7

Korogi, 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.

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8

Dysart, 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.

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Pulmonary fibrosis is a potentially deadly pathology characterized by excessive deposition of extracellular matrix (ECM), increased tissue stiffness, and loss of tissue structure and function. Recent evidence has suggested epithelial to mesenchymal transition (EMT), the transdifferentiation of an epithelial cell into a mesenchymal fibroblast, is one mechanism that results in the accumulation of myofibroblasts and excessive deposition of ECM. EMT is a highly orchestrated process involving the integration of biochemical signals from specific integrin mediated interactions with ECM proteins and s

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9

Doolittle, 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.

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10

Assis, 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/.

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Os eventos celulares e extracelulares que ocorrem durante o processo de osseointegração do titânio (Ti) são bastante influenciados por suas propriedades de superfície, como morfologia, topografia e composição química. A modificação bioquímica da superfície do Ti consiste em imobilizar proteínas ou peptídeos nessa superfície com a finalidade de induzir respostas celulares e teciduais específicas na interface osso-implante que acelerem ou aumentem a osseointegração. O objetivo deste estudo foi avaliar o desenvolvimento do fenótipo osteoblástico em culturas de células crescidas sobre Ti revestido

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11

VOLPE, MARIA CONCETTA. "miR-200c prevents and reverts Lung fibrosis by down regulating Flt1 and promoting lung regeneration." Doctoral thesis, Università degli Studi di Trieste, 2022. http://hdl.handle.net/11368/3014982.

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Idiopathic pulmonary fibrosis (IPF) is a devastating progressive fibrotic disease affecting the lungs and causing chronic respiratory failure. In IPF, adult alveolar type II stem cells (ATII) cannot trans-differentiate to alveolar type I cells (ATI), and therefore, represents a relevant target in the progression of lung fibrosis. There are only two FDA-approved drugs for the treatment of IPF, which can only ameliorate the disease, but a permanent cure is not yet available. In this work, we showed that human ATII cells isolated from IPF patients displayed impaired trans-differentiation in vitro

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12

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.

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13

Rako, 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.

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14

Rako, 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.

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15

Cherlet, 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.

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16

Kanj, 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.

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Thesis (Ph. D.)--West Virginia University, 2004.<br>Title from document title page. Document formatted into pages; contains x, 130 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 120-130).

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17

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.

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18

Sammohi, 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.

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19

Gereke, 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.

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20

Garrison, 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.

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21

Singer, 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.

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22

Samuels, 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.

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23

Marten, 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.

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24

Jacob, Anjali. "Generation of mature type II alveolar epithelial cells from human pluripotent stem cells." Thesis, 2017. https://hdl.handle.net/2144/26476.

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Tissues arising late in evolutionary time, such as lung alveoli that are unique to air breathing organisms, have been challenging to generate in vitro from pluripotent stem cells (PSCs), in part because there are limited lower organism model systems available to provide the necessary developmental roadmaps to guide in vitro differentiation. Furthermore, pulmonary alveolar epithelial type II cell (AEC2) dysfunction has been implicated as a primary cause of pathogenesis in many poorly understood lung diseases that lack effective therapies, including interstitial lung disease (ILD) and emphysema.

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25

Lo, 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.

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<p>Due 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 fun

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26

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.

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The most common causes of childhood interstitial lung disease (chILD) are autosomal recessive mutations in the gene encoding ATP Binding Cassette A3 (ABCA3) protein, a lamellar body (LB) associated lipid transporter exclusively expressed within the alveolar epithelial type II cells (AEC2s) in the lung. Instability of primary AEC2s in culture has prevented studies of ABCA3 mutations, resulting in limited understanding of disease pathogenesis. To overcome this challenge, we developed AEC2-like cells from human pluripotent stem cells (PSCs) in vitro, allowing study of normal ABCA3 function and pe

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27

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.

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碩士<br>國防醫學院<br>航太及海底醫學研究所<br>107<br>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/prog

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28

Merluza, John. "Nicotine and cotinine effects on fetal rat lung type II alveolar cells." 2006. http://hdl.handle.net/1993/20898.

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29

Lin, 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.

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碩士<br>輔仁大學<br>基礎醫學研究所碩士班<br>95<br>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 phosph

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30

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.

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碩士<br>國立中興大學<br>生物醫學研究所<br>94<br>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 metastas

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31

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.

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32

Gandhi, 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.

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33

Ahmed, 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.

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Exposure cigarette smoke (CS) during prenatal life is the leading cause of preventable premature death. In this study, we explored the hypothesis that in vitro exposure of fetal lung cells to cigarette smoke extract (CSE) may result in the alteration of apoptosis through activation of caspase-3. Alongside we compared the responses of fetal lung cells with A549 cells and rat periodontal ligament (PDL) fibroblasts exposed to CSE in a dose dependent manner. Caspase-3 activity and inhibition was measured using a fluorometric assay. Cell viability in smoke exposed cells was measured using MTT forma

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34

Chuang, 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.

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博士<br>臺北醫學大學<br>臨床醫學研究所<br>99<br>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 t

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35

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.

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The fetal lung secretes significant quantities of surfactant during late gestation in preparation for respiration which must begin immediately after birth. Although initiation of surfactant synthesis/secretion may be accelerated, the underlying mechanisms of the process itself remain to be resolved. An important pathway in adult lung has implicated the a$\sp{2+}$-PS-dependent enzyme protein kinase C (PKC) in its regulation. The present study was undertaken to characterize the activity of Ca$\sp{2+}$-PS-dependent PKC in adult lung and to determine if PKC was involved in the processes of initiat

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36

Chupin, Cécile. "Impact du stress oxydant sur les mécanismes de clairance alvéolaire et de réparation épithéliale pulmonaires." Thèse, 2008. http://hdl.handle.net/1866/7584.

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