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Journal articles on the topic 'Alveolar type cell'

Author: Grafiati

Published: 1 April 2023

Last updated: 31 July 2025

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1

Sutherland, Leanne M., Yasmin S. Edwards, and Andrew W. Murray. "Alveolar type II cell apoptosis." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 129, no. 1 (2001): 267–85. http://dx.doi.org/10.1016/s1095-6433(01)00323-3.

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2

Dormans, J. A. M. A. "The alveolar type III cell." Lung 163, no. 1 (1985): 327–35. http://dx.doi.org/10.1007/bf02713833.

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3

Griffin, M., R. Bhandari, G. Hamilton, Y. C. Chan, and J. T. Powell. "Alveolar type II cell-fibroblast interactions, synthesis and secretion of surfactant and type I collagen." Journal of Cell Science 105, no. 2 (1993): 423–32. http://dx.doi.org/10.1242/jcs.105.2.423.

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During alveolar development and alveolar repair close contacts are established between fibroblasts and lung epithelial cells through gaps in the basement membrane. Using co-culture systems we have investigated whether these close contacts influence synthesis and secretion of the principal surfactant apoprotein (SP-A) by cultured rat lung alveolar type II cells and the synthesis and secretion of type I collagen by fibroblasts. The alveolar type II cells remained cuboidal and grew in colonies on fibroblast feeder layers and on Matrigel-coated cell culture inserts but were progressively more flat

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4

Paine, R., P. Christensen, G. B. Toews, and R. H. Simon. "Regulation of alveolar epithelial cell ICAM-1 expression by cell shape and cell-cell interactions." American Journal of Physiology-Lung Cellular and Molecular Physiology 266, no. 4 (1994): L476—L484. http://dx.doi.org/10.1152/ajplung.1994.266.4.l476.

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In normal lung, intercellular adhesion molecule 1 (ICAM-1) is expressed at high levels on thin type I alveolar epithelial cells, but is minimally expressed on cuboidal type II cells. ICAM-1 is induced in primary culture on tissue culture-treated plastic as type II cells undergo transition toward a type I cell-like phenotype. We hypothesized that alveolar epithelial cell expression of ICAM-1 might be regulated in part by signals that influence the state of differentiation of these cells. We found that rat type II cells that were cultured as aggregates of cuboidal cells on a hydrated basement me

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5

Planus, E., S. Galiacy, M. Matthay, et al. "Role of collagenase in mediating in vitro alveolar epithelial wound repair." Journal of Cell Science 112, no. 2 (1999): 243–52. http://dx.doi.org/10.1242/jcs.112.2.243.

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Type II pneumocytes are essential for repair of the injured alveolar epithelium. The effect of two MMP collagenases, MMP-1 and MMP-13 on alveolar epithelial repair was studied in vitro. The A549 alveolar epithelial cell line and primary rat alveolar epithelial cell cultures were used. Cell adhesion and cell migration were measured with and without exogenous MMP-1. Wound healing of a cell monolayer of rat alveolar epithelial cell after a mechanical injury was evaluated by time lapse video analysis. Cell adhesion on type I collagen, as well as cytoskeleton stiffness, was decreased in the presenc

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6

Alder, Jonathan K., Christina E. Barkauskas, Nathachit Limjunyawong, et al. "Telomere dysfunction causes alveolar stem cell failure." Proceedings of the National Academy of Sciences 112, no. 16 (2015): 5099–104. http://dx.doi.org/10.1073/pnas.1504780112.

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Telomere syndromes have their most common manifestation in lung disease that is recognized as idiopathic pulmonary fibrosis and emphysema. In both conditions, there is loss of alveolar integrity, but the underlying mechanisms are not known. We tested the capacity of alveolar epithelial and stromal cells from mice with short telomeres to support alveolar organoid colony formation and found that type 2 alveolar epithelial cells (AEC2s), the stem cell-containing population, were limiting. When telomere dysfunction was induced in adult AEC2s by conditional deletion of the shelterin component telom

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7

Ashino, Yugo, Xiaoyou Ying, Leland G. Dobbs, and Jahar Bhattacharya. "[Ca2+]i oscillations regulate type II cell exocytosis in the pulmonary alveolus." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 1 (2000): L5—L13. http://dx.doi.org/10.1152/ajplung.2000.279.1.l5.

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Pulmonary surfactant, a critical determinant of alveolar stability, is secreted by alveolar type II cells by exocytosis of lamellar bodies (LBs). To determine exocytosis mechanisms in situ, we imaged single alveolar cells from the isolated blood-perfused rat lung. We quantified cytosolic Ca2+ concentration ([Ca2+]i) by the fura 2 method and LB exocytosis as the loss of cell fluorescence of LysoTracker Green. We identified alveolar cell type by immunofluorescence in situ. A 15-s lung expansion induced synchronous [Ca2+]i oscillations in all alveolar cells and LB exocytosis in type II cells. The

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8

Hammerschmidt, Stefan, Hartmut Kuhn, Christian Gessner, Hans-Jurgen Seyfarth, and Hubert Wirtz. "Stretch-Induced Alveolar Type II Cell Apoptosis." American Journal of Respiratory Cell and Molecular Biology 37, no. 6 (2007): 699–705. http://dx.doi.org/10.1165/rcmb.2006-0429oc.

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9

Patel, Namrata B., and Jason D. Christie. "Alveolar Type 2 Cell Transplantation in IPF." Chest 150, no. 3 (2016): 481–82. http://dx.doi.org/10.1016/j.chest.2016.05.036.

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10

Wang, P. M., E. Fujita, and J. Bhattacharya. "Vascular regulation of type II cell exocytosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 282, no. 5 (2002): L912—L916. http://dx.doi.org/10.1152/ajplung.00303.2001.

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To determine whether lung capillary pressure regulates surfactant secretion, we viewed alveoli of the constantly inflated, isolated blood-perfused rat lung by fluorescence microscopy. By alveolar micropuncture we infused fura 2 and lamellar body (LB)-localizing dyes for fluorescence detection of, respectively, the alveolar cytosolic Ca2+concentration ([Ca2+]i) and type II cell exocytosis. Increasing left atrial pressure (Pla) from 5 to 10 cmH2O increased septal capillary diameter by 26% and induced marked alveolar [Ca2+]i oscillations that abated on relief of pressure elevation. The rate of lo

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11

Sherwin, R. P., and V. Richters. "Image Analysis Quantitation of Type 2 Cells and Alveolar Walls Part I: Influence of Time on the Developing Mouse Lung." Journal of the American College of Toxicology 4, no. 1 (1985): 17–26. http://dx.doi.org/10.3109/10915818509014501.

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Quantitative measurements of the lungs of Swiss-Webster male mice at 6, 10, and 16 weeks of age were obtained using image analysis. The measurements included numbers and area of type 2 cells, and the area, perimeters, and linear intercepts of alveolar walls. In addition, type 2 cell:alveolar wall ratios were used to compare cell and alveolar wall interrelationships with time. The most outstanding of the findings was a 21.8% increase in mean type 2 cell area with time (6 weeks vs. 16 weeks of age; P < 0.05), with only a relatively slight increase (6.3%) in the number of type 2 cells. Type 2

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12

Wang, Yanjie, Zan Tang, Huanwei Huang, et al. "Pulmonary alveolar type I cell population consists of two distinct subtypes that differ in cell fate." Proceedings of the National Academy of Sciences 115, no. 10 (2018): 2407–12. http://dx.doi.org/10.1073/pnas.1719474115.

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Pulmonary alveolar type I (AT1) cells cover more than 95% of alveolar surface and are essential for the air–blood barrier function of lungs. AT1 cells have been shown to retain developmental plasticity during alveolar regeneration. However, the development and heterogeneity of AT1 cells remain largely unknown. Here, we conducted a single-cell RNA-seq analysis to characterize postnatal AT1 cell development and identified insulin-like growth factor-binding protein 2 (Igfbp2) as a genetic marker specifically expressed in postnatal AT1 cells. The portion of AT1 cells expressing Igfbp2 increases du

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13

Dobbs, L. G. "Isolation and culture of alveolar type II cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 258, no. 4 (1990): L134—L147. http://dx.doi.org/10.1152/ajplung.1990.258.4.l134.

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The alveolar type II cell performs many important functions within the lung, including regulation of surfactant metabolism, ion transport, and alveolar repair. Because type II cells comprise only 15% of all lung cells, it is difficult to attribute specific functions to type II cells from studies of whole lungs or mixed cell cultures. At the present time, there is no passaged line that exhibits the full range of known type II cell functions. For these reasons, investigators have used isolated type II cells to study alveolar cell biology, biochemistry, and molecular biology. This review addresse

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14

Rybicka, Krystyna. "Histogenesis of alveolar cell carcinoma." Proceedings, annual meeting, Electron Microscopy Society of America 45 (August 1987): 626–27. http://dx.doi.org/10.1017/s0424820100127566.

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Alveolar cell carcinoma (ACC) is a lung neoplasm characterized by the presence of lamellar bodies specific for normal type 2 alveolar cells. Tumor histogenesis is uncertain. The present study indicates that ACC originates from dedifferentiation of hyperplastic type 2 alveolar cells rather than migration of bronchial stem cells into alveoli as suggested earlier.An aliquot of human lung biopsy diagnosed as ACC was fixed in glutaraldehyde and osmium, treated with 1% aqueous uranyl acetate, and embedded in epoxy resin. Sections were stained for glycogen by periodic acid - thiosemicarbazide - silve

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15

Lee, Vivian Y., Clara Schroedl, Joslyn K. Brunelle, et al. "Bleomycin induces alveolar epithelial cell death through JNK-dependent activation of the mitochondrial death pathway." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 4 (2005): L521—L528. http://dx.doi.org/10.1152/ajplung.00340.2004.

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Exposure to bleomycin in rodents induces lung injury and fibrosis. Alveolar epithelial cell death has been hypothesized as an initiating mechanism underlying bleomycin-induced lung injury and fibrosis. In the present study we evaluated the contribution of mitochondrial and receptor-meditated death pathways in bleomycin-induced death of mouse alveolar epithelial cells (MLE-12 cells) and primary rat alveolar type II cells. Control MLE-12 cells and primary rat alveolar type II cells died after 48 h of exposure to bleomycin. Both MLE-12 cells and rat alveolar type II cells overexpressing Bcl-XLdid

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16

Beers, Michael F., and Yuben Moodley. "When Is an Alveolar Type 2 Cell an Alveolar Type 2 Cell? A Conundrum for Lung Stem Cell Biology and Regenerative Medicine." American Journal of Respiratory Cell and Molecular Biology 57, no. 1 (2017): 18–27. http://dx.doi.org/10.1165/rcmb.2016-0426ps.

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17

Castleman, W. L., P. J. Northrop, and P. K. McAllister. "Replication of parainfluenza type-3 virus and bovine respiratory syncytial virus in isolated bovine type-II alveolar epithelial cells." American Journal of Veterinary Research 52, no. 6 (1991): 880–85. http://dx.doi.org/10.2460/ajvr.1991.52.06.880.

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SUMMARY The objectives of our research were to determine whether bovine pulmonary type-II alveolar epithelial cells could be isolated from bovine lung and maintained in tissue culture and to determine whether isolated bovine type-II alveolar epithelial cells would support productive viral replication of bovine parainfluenza type-3 virus and bovine respiratory syncytial virus. Type-II alveolar epithelial cells were isolated from lungs of 4- to 7-day-old male Holstein calves by enzymatic dissociation of pulmonary tissue with trypsin and by separation of cells with the use of filtration and centr

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18

McElroy, M. C., J. F. Pittet, S. Hashimoto, L. Allen, J. P. Wiener-Kronish, and L. G. Dobbs. "A type I cell-specific protein is a biochemical marker of epithelial injury in a rat model of pneumonia." American Journal of Physiology-Lung Cellular and Molecular Physiology 268, no. 2 (1995): L181—L186. http://dx.doi.org/10.1152/ajplung.1995.268.2.l181.

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In this study we determined whether the alveolar fluid content of a specific epithelial type I cell protein, rTI40, can be used as a biochemical marker for lung injury. A model of alveolar epithelial injury was developed by instilling Pseudomonas aeruginosa bacteria (PA103) into the airspaces of anesthetized, ventilated rats. After 6 h, the alveolar fluid content of rTI40 from PA103-treated rats was increased over 80-fold in comparison to alveolar fluid from control rats (P < 0.05). This increase in rTI40 correlated with both morphological evidence of injury to alveolar epithelial type I ce

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19

Cott, G. R., K. Sugahara, and R. J. Mason. "Stimulation of net active ion transport across alveolar type II cell monolayers." American Journal of Physiology-Cell Physiology 250, no. 2 (1986): C222—C227. http://dx.doi.org/10.1152/ajpcell.1986.250.2.c222.

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The active transcellular transport of electrolytes across the alveolar epithelium probably plays an important role in alveolar fluid homeostasis by helping to maintain the alveolus relatively free of fluid. To better understand the factors regulating active ion transport across alveolar epithelial cells, we examined the effect of a number of pharmacologically active agents on the bioelectric properties of alveolar type II cells in primary culture. Alveolar type II cells were isolated from adult male rats and cultured on collagen-coated Millipore filters for 6-14 days. The bioelectric propertie

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20

Chen, Qian, Varsha Suresh Kumar, Johanna Finn, et al. "CD44high alveolar type II cells show stem cell properties during steady-state alveolar homeostasis." American Journal of Physiology-Lung Cellular and Molecular Physiology 313, no. 1 (2017): L41—L51. http://dx.doi.org/10.1152/ajplung.00564.2016.

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The alveolar epithelium is composed of type I cells covering most of the gas-blood exchange surface and type II cells secreting surfactant that lowers surface tension of alveoli to prevent alveolar collapse. Here, we have identified a subgroup of type II cells expressing a higher level of cell surface molecule CD44 (CD44high type II cells) that composed ~3% of total type II cells in 5–10-wk-old mice. These cells were preferentially apposed to lung capillaries. They displayed a higher proliferation rate and augmented differentiation capacity into type I cells and the ability to form alveolar or

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21

Miller, Marian L. "Anatomy of an Alveolar Type II Cell Diagram." Microscopy Today 25, no. 5 (2017): 30–35. http://dx.doi.org/10.1017/s1551929517000803.

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22

Donati, Yves, Sanja Blaskovic, Isabelle Ruchonnet-Métrailler, Josefina Lascano Maillard, and Constance Barazzone-Argiroffo. "Simultaneous isolation of endothelial and alveolar epithelial type I and type II cells during mouse lung development in the absence of a transgenic reporter." American Journal of Physiology-Lung Cellular and Molecular Physiology 318, no. 4 (2020): L619—L630. http://dx.doi.org/10.1152/ajplung.00227.2019.

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Mouse lung developmental maturation and final alveolarization phase begin at birth. During this dynamic process, alveolar cells modify their morphology and anchorage to the extracellular matrix. In particular, alveolar epithelial cell (AEC) type I undergo cytoplasmic flattening and folding to ensure alveoli lining. We developed FACS conditions for simultaneous isolation of alveolar epithelial and endothelial cells in the absence of specific reporters during the early and middle alveolar phase. We evidenced for the first time a pool of extractable epithelial cell populations expressing high lev

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23

Kim, H. J., D. H. Ingbar, and C. A. Henke. "Integrin mediation of type II cell adherence to provisional matrix proteins." American Journal of Physiology-Lung Cellular and Molecular Physiology 271, no. 2 (1996): L277—L286. http://dx.doi.org/10.1152/ajplung.1996.271.2.l277.

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Lung injury causes alveolar type I epithelial cell death, basement membrane denudation, and alveolar flooding with serum fibronectin and fibrinogen. For successful restoration of normal architecture, the epithelium must be regenerated from progenitor type II alveolar cells. Using adhesion assays, we examined whether type II alveolar cells adhere to the provisional matrix proteins fibronectin, fibrinogen, and fibrin, and whether integrins mediate this adherence. Rat type II cells adhered to fibronectin, vitronectin, fibrinogen, and fibrin. Synthetic RGD (arginine-glycine-aspartic acid) peptide

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24

Yang, Honghua, Min Min Lu, Lili Zhang, Jeffrey A. Whitsett, and Edward E. Morrisey. "GATA6 regulates differentiation of distal lung epithelium." Development 129, no. 9 (2002): 2233–46. http://dx.doi.org/10.1242/dev.129.9.2233.

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GATA6 is a member of the GATA family of zinc-finger transcriptional regulators and is the only known GATA factor expressed in the distal epithelium of the lung during development. To define the role that GATA6 plays during lung epithelial cell development, we expressed a GATA6-Engrailed dominant-negative fusion protein in the distal lung epithelium of transgenic mice. Transgenic embryos lacked detectable alveolar epithelial type 1 cells in the distal airway epithelium. These embryos also exhibited increased Foxp2 gene expression, suggesting a disruption in late alveolar epithelial differentiat

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Liu, Jianhua, Liqing Zheng, Liang Cao, Changhong Zhang, and Chen Li. "STAT3 Promotes Apoptosis of Alveolar Epithelial Cells by Inhibiting AKT Signaling." Tobacco Regulatory Science 7, no. 4 (2021): 741–48. http://dx.doi.org/10.18001/trs.7.4.1.28.

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Type II alveolar epithelial cells are a crucial component of alveolar epithelium, and transcriptional activator 3 (STAT3) have functions in regulating alveolar epithelial cell proliferation. Therefore, based on the modular approach, we analyzed the effects of silencing STAT3 on type II alveolar epithelial cells and studied its mechanism of action. Initially, in the GEO database, we downloaded data on type II alveolar epithelial cells. For transcript to me data in alveolar epithelial cell samples, we performed a differential analysis. Secondly, protein interaction network analysis (PPIs) were p

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Barton, W. W., S. E. Wilcoxen, P. J. Christensen, and R. Paine. "Association of ICAM-1 with the cytoskeleton in rat alveolar epithelial cells in primary culture." American Journal of Physiology-Lung Cellular and Molecular Physiology 271, no. 5 (1996): L707—L718. http://dx.doi.org/10.1152/ajplung.1996.271.5.l707.

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Intercellular adhesion molecule-1 ICAM-1) is a transmembrane adhesion protein that is expressed constitutively on the apical surface of type I cells in vivo and on type II cells in vitro as they spread in culture, assuming type I cell-like characteristics. To investigate the possible interaction of ICAM-1 with the alveolar epithelial cell cytoskeleton, rat type II cells in primary culture were extracted with nonionic detergent, and residual ICAM-1 associated with the cytoskeletal remnants was determined using immunofluorescence microscopy, immunoprecipitation, and cell-based enzyme-linked immu

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Cao, Chao, Obulkasim Memete, Yiru Shao, et al. "Single-Cell RNA-Sequencing Reveals Epithelial Cell Signature of Multiple Subtypes in Chemically Induced Acute Lung Injury." International Journal of Molecular Sciences 24, no. 1 (2022): 277. http://dx.doi.org/10.3390/ijms24010277.

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Alveolar epithelial cells (AECs) play a role in chemically induced acute lung injury (CALI). However, the mechanisms that induce alveolar epithelial type 2 cells (AEC2s) to proliferate, exit the cell cycle, and transdifferentiate into alveolar epithelial type 1 cells (AEC1s) are unclear. Here, we investigated the epithelial cell types and states in a phosgene-induced CALI rat model. Single-cell RNA-sequencing of bronchoalveolar lavage fluid (BALF) samples from phosgene-induced CALI rat models (Gas) and normal controls (NC) was performed. From the NC and Gas BALF samples, 37,245 and 29,853 high

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Auten, Richard L., S. Nicholas Mason, Kathryn M. Auten, and Mulugu Brahmajothi. "Hyperoxia impairs postnatal alveolar epithelial development via NADPH oxidase in newborn mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 297, no. 1 (2009): L134—L142. http://dx.doi.org/10.1152/ajplung.00112.2009.

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Hyperoxia disrupts postnatal lung development in part through inducing inflammation. To determine the contribution of leukocyte-derived reactive oxygen species, we exposed newborn wild-type and NADPH oxidase p47 phox subunit null (p47 phox−/−) mice to air or acute hyperoxia (95% O2) for up to 11 days. Hyperoxia-induced pulmonary neutrophil influx was similar in wild-type and p47−/− mice at postnatal days (P) 7 and 11. Macrophages were decreased in wild-type hyperoxia-exposed mice compared with p47 phox−/− mice at P11. Hyperoxia impaired type II alveolar epithelial cell and bronchiolar epitheli

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Nicholas, TE. "Control of Turnover of Alveolar Surfactant." Physiology 8, no. 1 (1993): 12–18. http://dx.doi.org/10.1152/physiologyonline.1993.8.1.12.

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Surfactant is released from alveolar type II cells into a hypophase where it modifies surface tension and stabilizes alveoli. It is then taken back into the type II cell and reutilized. Although many secretagogues are suggested, the major release stimulus is probably distrotion of the type II cell.

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Tang, Chong-Ti, Yan-Hai Wang, Wen-Feng Peng, Liang Tang, and Dong Chen. "ALVEOLAR ECHINOCOCCUS SPECIES FROM VULPES CORSAC IN HULUNBEIER, INNER MONGOLIA, CHINA, AND DIFFERENTIAL DEVELOPMENT OF THE METACESTODES IN EXPERIMENTAL RODENTS." Journal of parasitology 92, no. 4 (2006): 719–24. https://doi.org/10.1645/GE-3526.1.

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Adults of alveolar Echinococcus species with different uterine structures were collected from Vulpes corsac in the Hulunbeier Pasture of Northeastern China in 2001. They were Echinococcus multilocularis Leuckart, 1863 (type No. 3, similar to E. m. multilocularis), with vaselike uterus; Echinococcus cf. sibiricensis Rausch et Schiller, 1954 (type No. 1), with pyriform uterus; and Echinococcus sp. (type No. 2) with spherical uterus at segment top. The metacestode development in rodents also differed among those 3 parasites. In the case of E. multilocularis (type No. 3), many germinal cells grew

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Abdelwahab, Elhusseiny Mohamed Mahmud, Judit Rapp, Diana Feller, et al. "Wnt signaling regulates trans-differentiation of stem cell like type 2 alveolar epithelial cells to type 1 epithelial cells." Respiratory Research 20, no. 1 (2019): 204. https://doi.org/10.1186/s12931-019-1176-x.

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<strong>Background: </strong>Type 2 alveolar epithelial cells (AT2s) behave as stem cells and show clonal proliferation upon alveolar injury followed by trans-differentiation (TD) into Type 1 alveolar epithelial cells (AT1s). In the present study we identified signaling pathways involved in the physiological AT2-to-AT1 TD process.<strong>Methods: </strong>AT2 cells can be isolated from human lungs and cultured in vitro where they undergo TD into AT1s. In the present study we identified signaling pathways involved in the physiological AT2-to-AT1 TD process using Affymetrix microarray, qRT-PCR,

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Housset, B., I. Hurbain, J. Masliah, et al. "Toxic effects of oxygen on cultured alveolar epithelial cells, lung fibroblasts and alveolar macrophages." European Respiratory Journal 4, no. 9 (1991): 1066–75. http://dx.doi.org/10.1183/09031936.93.04091066.

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Exposure to hyperoxia results in endothelial necrosis followed by type II cell proliferation. This suggests that type II cells are resistant to hyperoxia. Oxygen-induced lung injury may result from an overproduction of oxygen metabolites normally scavenged by antioxidants such as superoxide dismutase (SOD), glutathione peroxidase, catalase and reduced glutathione (GSH). Therefore, resistance of type II cells to hyperoxia may be linked to high antioxidant activities. To test this hypothesis we compared in vitro the effects of a 24 h exposure period to 95% O2 on cultured type II cells, lung fibr

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Maniscalco, William M., Richard H. Watkins, Patricia R. Chess, Robert A. Sinkin, Stuart Horowitz, and Liana Toia. "Cell-specific expression of fibronectin and EIIIA and EIIIB splice variants after oxygen injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 274, no. 4 (1998): L599—L609. http://dx.doi.org/10.1152/ajplung.1998.274.4.l599.

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Cellular fibronectin (cFN) expression is characteristic of injured tissues. Unlike plasma FN, cFN mRNA often contains the EIIIA or EIIIB domains. We examined the lung cell-specific expression of total cFN mRNA and the EIIIA and EIIIB splice variants in rabbits after acute oxygen injury. By in situ hybridization, control lung had low cFN mRNA. After exposure to >95% oxygen, mRNAs for total cFN and EIIIA were noted primarily in alveolar macrophages and large-vessel endothelial cells. By 3–5 days recovery, cFN and EIIIA mRNA abundance was increased in alveolar septal cells (i.e., alveolar epit

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Hoshino, Yuma, Tadashi Mio, Sonoko Nagai, Hiroyuki Miki, Isao Ito, and Takateru Izumi. "Cytotoxic effects of cigarette smoke extract on an alveolar type II cell-derived cell line." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 2 (2001): L509—L516. http://dx.doi.org/10.1152/ajplung.2001.281.2.l509.

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Injury of the alveolar epithelium by cigarette smoke is presumed to be an important process in the pathogenesis of smoking-related pulmonary diseases. We investigated the cytotoxic effects of cigarette smoke extract (CSE) on an alveolar type II cell-derived cell line (A549). CSE caused apoptosis at concentrations of 5% or less and necrosis at 10% or more. When CSE was exposed to air before application to A549 cells, the cytotoxic effects were attenuated. CSE caused cell death without direct contact with the cells. Acrolein and hydrogen peroxide, two major volatile factors in cigarette smoke, c

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Fine, A., N. L. Anderson, T. L. Rothstein, M. C. Williams, and B. R. Gochuico. "Fas expression in pulmonary alveolar type II cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 273, no. 1 (1997): L64—L71. http://dx.doi.org/10.1152/ajplung.1997.273.1.l64.

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Fas, a type I membrane receptor protein, transduces a signal culminating in apoptosis after binding to the Fas ligand. Information regarding the expression of Fas in nonlymphoid tissues, although limited, suggests a role for Fas in epithelial progenitor cell populations. In this paper, we provide several lines of evidence indicating that the progenitor cell of the alveolus, the type II cell, displays restricted expression of Fas. We found 1) Fas gene expression in RNA derived from fresh isolates of primary rat type II cells; 2) restriction of Fas expression to a subset of alveolar type II cell

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Bolt, M. W., W. J. Racz, J. F. Brien, T. M. Bray, and T. E. Massey. "Differential susceptibilities of isolated hamster lung cell types to amiodarone toxicity." Canadian Journal of Physiology and Pharmacology 76, no. 7-8 (1998): 721–27. http://dx.doi.org/10.1139/y98-084.

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Treatment of cardiac dysrhythmias with the iodinated benzofuran derivative amiodarone (AM) is limited by pulmonary toxicity. The susceptibilities of different lung cell types of male Golden Syrian hamsters to AM-induced cytotoxicity were investigated in vitro. Bronchoalveolar lavage and protease digestion to release cells, followed by centrifugal elutriation and density gradient centrifugation, resulted in preparations enriched with alveolar macrophages (98%), alveolar type II cells (75-85%), and nonciliated bronchiolar epithelial (Clara) cells (35-50%). Alveolar type II cell and Clara cell pr

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Cott, G. R. "Modulation of bioelectric properties across alveolar type II cells by substratum." American Journal of Physiology-Cell Physiology 257, no. 4 (1989): C678—C688. http://dx.doi.org/10.1152/ajpcell.1989.257.4.c678.

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Rat alveolar type II cells were cultured on collagen-coated filters (CCF) and human amnionic basement membrane (ABM) to determine the effect of culture substratum on the development of monolayer bioelectric properties. Monolayers cultured on both substrata rapidly developed bioelectric properties with similar time courses, monolayer capacitance values (approximately 1 muF/cm2), current-voltage relationships, and responses to stimulants and inhibitors of active ion transport. Increasing seeding densities tended to increase monolayer bioelectric properties regardless of culture substratum. Monol

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Mensah, E. A., N. M. Kumar, L. Nielsen, and J. S. Lwebuga-Mukasa. "Distribution of alveolar type II cells in neonatal and adult rat lung revealed by RT-PCR in situ." American Journal of Physiology-Lung Cellular and Molecular Physiology 271, no. 1 (1996): L178—L185. http://dx.doi.org/10.1152/ajplung.1996.271.1.l178.

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Type II pneumocytes in newborn lungs are more uniformly distributed, whereas in adult lungs they are located at alveolar corners. We used morphometry and reverse transcription-polymerase chain reaction in situ hybridization of surfactant protein C mRNA to determine the patterns of type II cell distribution in random lung sections from Sprague-Dawley rats at various neonatal stages and adults. There was a progressive increase in the percentage of type II cells at alveolar corners from 30% at 1 day to 51, 62, 78, and 81% at 3, 5, and 7 days old and adult rats, respectively. There were statistica

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Yee, Min, Peter F. Vitiello, Jason M. Roper, et al. "Type II epithelial cells are critical target for hyperoxia-mediated impairment of postnatal lung development." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 5 (2006): L1101—L1111. http://dx.doi.org/10.1152/ajplung.00126.2006.

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Type II epithelial cells are essential for lung development and remodeling, as they are precursors for type I cells and can produce vascular mitogens. Although type II cell proliferation takes place after hyperoxia, it is unclear why alveolar remodeling occurs normally in adults whereas it is permanently disrupted in newborns. Using a line of transgenic mice whose type II cells could be identified by their expression of enhanced green fluorescent protein and endogenous expression of surfactant proteins, we investigated the age-dependent effects of hyperoxia on type II cell proliferation and al

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Ryan, R. M., M. M. Mineo-Kuhn, C. M. Kramer, and J. N. Finkelstein. "Growth factors alter neonatal type II alveolar epithelial cell proliferation." American Journal of Physiology-Lung Cellular and Molecular Physiology 266, no. 1 (1994): L17—L22. http://dx.doi.org/10.1152/ajplung.1994.266.1.l17.

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The type II alveolar epithelial cell plays a critical role in the repair of lung injury by repopulating the entire damaged alveolar epithelium. We report our studies of the effects of known growth factors on the in vitro proliferation of isolated neonatal rabbit type II cells. Transforming growth factor-alpha (TGF-alpha) and epidermal growth factor (EGF) increased [3H]thymidine incorporation, cell number, and labeling index above control. Transforming growth factor-beta (TGF-beta) decreased [3H]thymidine incorporation, cell number, and labeling index compared with control. When added simultane

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Wang, Chen, Feilong Hei, Zhihai Ju, Jie Yu, Shengnan Yang, and Mengmeng Chen. "Differentiation of Urine-Derived Human Induced Pluripotent Stem Cells to Alveolar Type II Epithelial Cells." Cellular Reprogramming 18, no. 1 (2016): 30–36. http://dx.doi.org/10.1089/cell.2015.0015.

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Poelma, D. L. H., L. J. I. Zimmermann, H. H. Scholten, B. Lachmann, and J. F. van Iwaarden. "In vivo and in vitro uptake of surfactant lipids by alveolar type II cells and macrophages." American Journal of Physiology-Lung Cellular and Molecular Physiology 283, no. 3 (2002): L648—L654. http://dx.doi.org/10.1152/ajplung.00478.2001.

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The uptake of fluorescent-labeled liposomes (with a surfactant-like composition) by alveolar macrophages and alveolar type II cells was studied using flow cytometry, in vivo by instillation of the labeled liposomes in the trachea of ventilated rats followed by isolation of the alveolar cells and determination of the cell-associated fluorescence, and in vitro by incubation of isolated alveolar cells with the fluorescent liposomes. The results show that the uptake of liposomes by the alveolar cells is time and concentration dependent. In vivo alveolar macrophages internalize more than three time

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Kalina, Moshe, and Shoshana Riklis. "Alveolar type II-like cell colonies: effect of alveolar macrophages and macrophage-conditioned media." Cell Differentiation 23, no. 3 (1988): 231–36. http://dx.doi.org/10.1016/0045-6039(88)90076-0.

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Simon, R. H., T. J. Gross, J. A. Edwards, and R. G. Sitrin. "Fibrin degradation by rat pulmonary alveolar epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 262, no. 4 (1992): L482—L488. http://dx.doi.org/10.1152/ajplung.1992.262.4.l482.

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The persistence of intra-alveolar fibrin during acute and chronic inflammatory lung diseases indicates that the normally profibrinolytic environment of the alveolar space has been altered as part of the disease process. We have recently shown that alveolar epithelial cells may control fibrinolysis by expressing both urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor-1. In this study, monolayers of rat alveolar epithelial cells were used as a model of the alveolar surface and were found to lyse plasma-derived fibrin matrices by a process that was plasminogen and uPA

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Tamò, Luca, Youssef Hibaoui, Sampada Kallol, et al. "Generation of an alveolar epithelial type II cell line from induced pluripotent stem cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 315, no. 6 (2018): L921—L932. http://dx.doi.org/10.1152/ajplung.00357.2017.

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Differentiation of primary alveolar type II epithelial cells (AEC II) to AEC type I in culture is a major barrier in the study of the alveolar epithelium in vitro. The establishment of an AEC II cell line derived from induced pluripotent stem cells (iPSC) represents a novel opportunity to study alveolar epithelial cell biology, for instance, in the context of lung injury, fibrosis, and repair. In the present study, we generated long-lasting AEC II from iPSC (LL-iPSC-AEC II). LL-iPSC-AEC II displayed morphological characteristics of AEC II, including growth in a cobblestone monolayer, the prese

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Kheradmand, F., H. G. Folkesson, L. Shum, R. Derynk, R. Pytela, and M. A. Matthay. "Transforming growth factor-alpha enhances alveolar epithelial cell repair in a new in vitro model." American Journal of Physiology-Lung Cellular and Molecular Physiology 267, no. 6 (1994): L728—L738. http://dx.doi.org/10.1152/ajplung.1994.267.6.l728.

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Alveolar epithelial type II cells are essential for regenerating an intact alveolar barrier after destruction of type I cells in vivo. The first objective of these experimental studies was to develop an in vitro model to quantify alveolar epithelial cell wound repair. The second objective was to investigate mechanisms of alveolar epithelial cell wound healing by studying the effects of serum and transforming growth factor-alpha (TGF-alpha) on wound closure. Primary cultures of rat alveolar type II cells were prepared by standard methods and grown to form confluent monolayers in 48 h. Then a wo

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Witherden, Ian R., Elizabeth J. Vanden Bon, Peter Goldstraw, Cathy Ratcliffe, Ugo Pastorino, and Teresa D. Tetley. "Primary Human Alveolar Type II Epithelial Cell Chemokine Release." American Journal of Respiratory Cell and Molecular Biology 30, no. 4 (2004): 500–509. http://dx.doi.org/10.1165/rcmb.4890.

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Seitz, Daniel H., Mario Perl, Stefanie Mangold, et al. "PULMONARY CONTUSION INDUCES ALVEOLAR TYPE 2 EPITHELIAL CELL APOPTOSIS." Shock 30, no. 5 (2008): 537–44. http://dx.doi.org/10.1097/shk.0b013e31816a394b.

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Sanchez-Esteban, Juan, Lawrence A. Cicchiello, Yulian Wang, et al. "Mechanical stretch promotes alveolar epithelial type II cell differentiation." Journal of Applied Physiology 91, no. 2 (2001): 589–95. http://dx.doi.org/10.1152/jappl.2001.91.2.589.

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Functional maturation of pulmonary alveolar epithelial cells is crucial for extrauterine survival. Mechanical distension and mesenchymal-epithelial interactions play important roles in this process. We hypothesized that mechanical stretch simulating fetal breathing movements is an important regulator of pulmonary epithelial cell differentiation. Using a Flexercell Strain Unit, we analyzed effects of stretch on primary cultures of type II cells and cocultures of epithelial and mesenchymal cells isolated from fetal rat lungs during late development. Cyclic stretch of isolated type II cells incre

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Crittenden, D. J., L. A. Alexander, and D. L. Beckman. "Sympathetic nerve influence on alveolar type II cell ultrastructure." Life Sciences 55, no. 15 (1994): 1229–35. http://dx.doi.org/10.1016/0024-3205(94)00662-8.

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