Dissertations / Theses: 'Alveolar type cell'

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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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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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. Developing cell culture models to study age-related effects of cigarette smoke on alveolar type I cells and microvascular endothelial cells from the lung, and 2. Using these models to examine the effects of CSE on markers of oxidative stress, inflammation and aging in alveolar cells harvested from neonatal, young and old rats. Descriptive and experimental studies involved using a variety of cell culture, biochemical and molecular techniques, including gene expression arrays. The most significant findings were that: 1. primary proliferating alveolar type I cells were used to develop novel cell culture model systems, including single culture, co-culture and three-dimensional cultures that were used to study the effects of CSE; 2. Hydrogen peroxide production by endothelial cells was markedly reduced by co-culturing with AT I cells; 3. Gene expression profiling of oxidative stress-specific pathways suggest that genes responsible for both stopping production of H2O2 or mopping-up H2O2 are involved; and 4. Cigarette smoke shortens telomeres of cells from neonates, but unexpectedly preserves telomere length of cells from young and old rats. Data from telomeric pathway-specific gene expression arrays suggest that there are age-related differences in response to gene expression to CSE. The significant conclusions are: 1. Contrary to prior observations, alveolar type I cells demonstrate prolonged proliferative capacity; 2. Alveolar type I cells likely play an important role in ameliorating CSE-induced oxidative stress; and 3. Neonatal alveolar cells may be more susceptible to the deleterious effects of CSE including telomere shortening. These novel model systems and observations provide new ways to study cigarette smoke-associated lung dysfunction.

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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 (Po) changed from 0.36 +/- 0.09 to 0.11 +/- 0.02; n=10, p=0.01 following CSE and DPI exposure. Likewise, Fulvene-5 (which inhibits Nox2 and Nox4 isoforms) decreased the number of ENaC per patch (from 2.75 +/- 0.25 to 1 +/- 0.5, n=9, p=0.002) and open probability (0.18 +/- 0.08 to 0.02 +/- 0.08, p=0.04). Cycloheximide chase assays show that CSE exposure prevented alpha-ENaC subunit degradation, whereas concurrent CSE exposure in the presence of Nox inhibitor, Fulvene 5, resulted in normal proteolytic degradation of alpha-ENaC protein in primary isolated lung cells. In vivo, co-instillation of CSE and Nox inhibitor promoted alveolar flooding in C57Bl6 mice compared to accelerated rates of fluid clearance observed in CSE alone instilled lungs. Real-time PCR indicates that mRNA levels of Nox2 were unaffected by CSE treatment while Nox4 transcript levels significantly increased 3.5 fold in response to CSE. Data indicate that CSE is an agonist of Nox4 enzymatic activity, and that CSE-mediated Nox4 plays an important role in altering lung ENaC activity.

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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. aureus-injured lungs also contained cells that co-stained-with a unique combination of ATI and ATII cell proteins, RTI40 and MMC4. To determine whether RTI40/MMC4-positive cells were likely to be intermediates in the transition of ATII to ATI cells I examined ATII cells as they transformed to ATI-like cells in culture (day 0 to 5). Only cells on day 1 of culture were RTI40/MMC4 positive. I also examined the developing lung for RT140/MC40 positive cells. Co-staining cells were not found in the developing alveolar epithelium, but they were present in small airways. I also developed a rat model of haemorrhagic shock induced ‘indirect’ alveolar epithelial injury as a platform for future work. Here I have developed a robust technique for imaging ATII cell transdifferentiation in vivo and in vitro. This work has identified a novel alveolar epithelial phenotype, RTI40/MMC4, in repairing lungs and in ATII cells as they transdifferentiate to ATI-like cells in vitro. These data suggest that RTI40/MMC4-positive cells can be used to both visualise alveolar epithelial intermediates in vivo and to investigate the regulation of ATII cell transdifferentiation following injury.

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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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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 soluble growth factors including TGFβ. TGFβ, a potent inducer of EMT, can be activated by cell contraction mediated mechanical release of the growth factor from a macromolecular latent complex. Therefore, TGFβ activity and subsequent EMT may be influenced by both the biochemical composition and biophysical state of the surrounding ECM. Based on these knowns it was first investigated how changes in the biochemical composition of the matrix and changes in tissue rigidity together modulate EMT due to changes in epithelial cell contraction and TGFβ activation. Here we show that integrin specific interactions with fibronectin (Fn) variants displaying both the RGD and PHSRN binding sites facilitate cell binding through α3β1 and α5β1 integrins, and that these interactions maintain an epithelial phenotype despite engagement of increased tissue rigidities. Conversely, Fn fragments that facilitate cell binding through αv integrins drive TGFβ activation and subsequent EMT even while engaging soft underlying substrates. Adding to the complexity of studying mechanisms that contribute to pulmonary fibrosis, is exposure of the lung to injuries from environmental particulates. Therefore, we investigated how EMT is altered in response to particulate matter (PM). Here we show that PM exposure further drives TGFβ activation, EMT, and increases intracellular levels of reactive oxygen species (ROS). Additionally, cells binding the ECM through α5β1 and α3β1 integrins only partially recover an epithelial phenotype, suggesting ROS may be a secondary driver of TGFβ and EMT. Taken together these results suggest dynamic changes to the ECM microenvironment are major contributors to the control of EMT responses and provide insights into the design of biomaterial-based microenvironments for control of epithelial cell phenotype.

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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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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 com colágeno tipo I. Para tanto, células osteoblásticas derivadas de fragmentos ósseos do processo alveolar de humanos foram cultivadas sobre discos de Ti usinados revestidos (Ti-col) ou não (Ti-usinado) com colágeno tipo I e foram avaliados os seguintes parâmetros: adesão, morfologia e proliferação celulares, síntese de proteína total, atividade de fosfatase alcalina (ALP), formação de matriz mineralizada, e expressão de genes marcadores do fenótipo osteoblástico por reação em cadeia da polimerase em tempo real (PCR em tempo real). O Ti-col alterou o crescimento e a expressão gênica das culturas e não teve efeito na adesão e morfologia celulares, síntese de proteína total, atividade de ALP e formação de matriz mineralizada comparado ao Ti-usinado. Esses resultados indicam que a superfície Ti-col pode favorecer um maior crescimento da cultura durante a fase proliferativa e um aumento e/ou aceleração da diferenciação, como indicado por alterações na expressão gênica de marcadores do fenótipo osteoblástico. Portanto, essa modificação de superfície pode ter um impacto nos processos de reparo e remodelação do tecido ósseo adjacente a implantes, favorecendo a ocorrência de maior formação óssea.
Cellular 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.

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11

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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12

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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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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14

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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15

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.
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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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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17

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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18

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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19

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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20

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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21

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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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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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. Here we report the successful directed differentiation in vitro of human PSCs into AEC2s, the facultative progenitors of lung alveoli. Using gene editing to engineer multicolored fluorescent reporter PSC lines (NKX2-1GFP;SFTPCtdTomato), we track and purify human SFTPC+ alveolar progenitors as they emerge from NKX2-1+ endodermal developmental precursors in response to stimulation of Wnt and FGF signaling. Purified PSC-derived SFTPC+ cells are able to form monolayered epithelial spheres (“alveolospheres”) in 3D cultures without the need for mesenchymal co-culture support, exhibit extensive self-renewal capacity, and display additional canonical AEC2 functional capacities, including innate immune responsiveness, the production of lamellar bodies able to package surfactant, and the ability to undergo squamous cell differentiation while upregulating type 1 alveolar cell markers. Guided by time-series global transcriptomic profiling we find that AEC2 maturation involves downregulation of Wnt signaling activity, and the highest differentially expressed transcripts in the resulting SFTPC+ cells encode genes associated with lamellar body and surfactant biogenesis. Finally, we apply this novel model system to generate patient-specific AEC2s from induced PSCs (iPSCs) carrying homozygous surfactant mutations (SFTPB121ins2), and we employ footprint-free CRISPR-based gene editing to observe that correction of this genetic lesion restores surfactant processing in the cells responsible for their disease. Thus we provide an approach for disease modeling and future functional regeneration of a cell type unique to air-breathing organisms.

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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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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 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.

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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 perturbations that result from ABCA3 mutations. To develop an AEC2 model that would recapitulate ABCA3 biology, we targeted human PSC lines with a knock-in GFP fusion reporter (ABCA3:GFP). Differentiations of PSCs into AEC2s (iAEC2s) resulted in exclusive expression of ABCA3:GFP in iAEC2s and intracellular localization to LAMP3+ vesicles, reminiscent of endogenous ABCA3. Moreover, we find these ABCA3:GFP+ iAEC2s express LBs, process surfactant proteins, and secret surfactant lipids, indicative of preserved ABCA3 function. To study the effects of ABCA3 mutations using our model, we generated two sets of PSC reporter lines: 1) two patient-derived iPSC lines carrying rare homozygous E690K and W308R ABCA3 mutations predicted to affect ABCA3 function or trafficking, respectively, and their two syngeneic gene-corrected lines each targeted with the AEC2-specific knock-in fluorescent reporter SFTPCtdTomato; and 2) three syngeneic ABCA3:GFP knock-in iPSC lines encoding wildtype, E690K, or W308R proteins. Directed differentiation of patient iPSCs into iAEC2s revealed attenuated secretion of surfactant-specific lipids, recapitulating clinical findings of surfactant deficiency. Examination of ABCA3 protein trafficking using the ABCA3:GFP fusion reporter revealed retained E690K and W308R mutant ABCA3 protein processing and trafficking compared to the wildtype protein by confocal microscopy and western blot analyses, however mutant iAEC2s exhibited smaller LBs, indicative of defective ABCA3-dependent lipid transport. Bulk RNA sequencing of mutant and gene-corrected SFTPCtdTomato- or ABCA3:GFP-expressing iAEC2s revealed enrichment of the TNF𝛼-NF𝜅B pathway in both W308R and E690K mutant iAEC2s, validated by lentiviral reporter assays and secretion of NF𝜅B-driven cytokines. Thus, we provide insights into how ABCA3 mutations alter AEC2 physiology and developed a platform to study other genetic AEC2 diseases through our ABCA3:GFP reporter system.
2021-05-26T00:00:00Z

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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
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.

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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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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
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.

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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
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.

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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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31

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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32

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 formazan assay. Caspase-3 expression and cellular localization was detected by western blot analysis and immunofluorescence. Our results indicate that caspase-3 activity was significantly (p < 0.05) elevated and cell viability was significantly inhibited in fetal rat lung cells exposed to 10% or 15 % (v/v) CSE. No significant differences were observed in the caspase-3 activity or cellular viability in A549 cells and rat PDL fibroblasts exposed to 5%, 10% or 15% (v/v) CSE. Activation of caspase-3 in fetal lung connective tissue and alveolar epithelial cells may be one of the reasons for the developmental pulmonary toxicity induced by CSE.

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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
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.

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34

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 initiation of synthesis and secretion of surfactant-related compounds in fetal and neonate lung. Protein and phospholipid levels, and activity profiles of Ca$\sp{2+}$-PS-dependent PKC were determined from subcellular fractions of fetal, neonate and adult rabbit lung. The enzyme's activity in the lamellar body fraction from whole lung and isolated type II cells was examined in greater detail. Additionally, the effect of PKC activation on uptake and release of phosphotidylcholine precursors $\lbrack\sp{32}$P) and $\lbrack\sp3$H) choline by isolated fetal type II pneumocytes was observed using the PKC activator tetradecanoylphorbol acetate (TPA). (Abstract shortened by UMI.)

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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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