Journal articles: 'Alveolar type cell'

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Chen, Qian, Varsha Suresh Kumar, Johanna Finn, Dianhua Jiang, Jiurong Liang, You-yang Zhao, and Yuru Liu. "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 (July 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 organoids compared with CD44low type II cells. Moreover, in aged mice, 18–24 mo old, the percentage of CD44high type II cells among all type II cells was increased, but these cells showed decreased progenitor properties. Thus CD44high type II cells likely represent a type II cell subpopulation important for constitutive regulation of alveolar homeostasis.

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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 (May 1, 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 loss of LB fluorescence that reflects the LB exocytosis rate increased fourfold after the pressure elevation and continued at the same rate even after pressure and [Ca2+]i oscillations had returned to baseline. In alveoli pretreated with either 1,2-bis(2-aminophenoxy)ethane- N,N,N′,N′-tetraacetic acid-AM, the intracellular Ca2+ chelator, or heptanol, the gap junctional blocker, the pressure-induced exocytosis was completely inhibited. We conclude that capillary pressure and surfactant secretion are mechanically coupled. The secretion initiates in a Ca2+-dependent manner but is sustained by Ca2+-independent mechanisms.

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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 (May 2001): 267–85. http://dx.doi.org/10.1016/s1095-6433(01)00323-3.

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

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Hall, Joshua D., Robin R. Craven, James R. Fuller, Raymond J. Pickles, and Thomas H. Kawula. "Francisella tularensis Replicates within Alveolar Type II Epithelial Cells In Vitro and In Vivo following Inhalation." Infection and Immunity 75, no. 2 (November 6, 2006): 1034–39. http://dx.doi.org/10.1128/iai.01254-06.

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ABSTRACT Francisella tularensis replicates in macrophages and dendritic cells, but interactions with other cell types have not been well described. F. tularensis LVS invaded and replicated within alveolar epithelial cell lines. Following intranasal inoculation of C57BL/6 mice, Francisella localized to the alveolus and replicated within alveolar type II epithelial cells.

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Wang, Yanjie, Zan Tang, Huanwei Huang, Jiao Li, Zheng Wang, Yuanyuan Yu, Chengwei Zhang, 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 (February 20, 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 during alveologenesis and in post pneumonectomy (PNX) newly formed alveoli. We found that the adult AT1 cell population contains both Hopx+Igfbp2+ and Hopx+Igfbp2− AT1 cells, which have distinct cell fates during alveolar regeneration. Using an Igfbp2-CreER mouse model, we demonstrate that Hopx+Igfbp2+ AT1 cells represent terminally differentiated AT1 cells that are not able to transdifferentiate into AT2 cells during post-PNX alveolar regeneration. Our study provides tools and insights that will guide future investigations into the molecular and cellular mechanism or mechanisms underlying AT1 cell fate during lung development and regeneration.

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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 - silver proteinate, and post-stained by uranyl acetate and lead citrate.The tumor contained morphologically distinct cell clusters. Each cluster consisted of identical cells. Differences between clusters resulted from synchronous alterations in lamellar bodies, mitochondria, glycosomes, and ribosomes. These alterations revealed distinct stages in cell differentiation classified here as follows: stage 1-hyperplastic cells (Fig.1), stage 2-dedifferentiating cells (Fig.2), stage 3-undifferentiated cells (Fig.3), stage 4-differentiating cells (Fig.4).

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Ichimura, Hideo, Kaushik Parthasarathi, Jens Lindert, and Jahar Bhattacharya. "Lung surfactant secretion by interalveolar Ca2+ signaling." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 4 (October 2006): L596—L601. http://dx.doi.org/10.1152/ajplung.00036.2006.

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Although clusters of alveoli form the acinus, which is the most distal respiratory unit, it is not known whether interalveolar communication coordinates acinar surfactant secretion. To address this, we applied real-time digital imaging in conjunction with photo-excited Ca2+ uncaging in intact alveoli of the isolated, blood-perfused rat lung. We loaded alveolar cells with the Ca2+ cage o-nitrophenyl EGTA-AM (NP-EGTA-AM) together with the fluorophores, fluo 4, or LysoTracker green (LTG) to determine, respectively, the cytosolic Ca2+ concentration ([Ca2+]cyt) or type 2 cell secretion. To uncage Ca2+ from NP-EGTA, we exposed a region in a selected alveolus to high-intensity UV illumination. As a result, fluo 4 fluorescence increased, whereas LTG fluorescence decreased, in the photo-targeted region, indicating that uncaging both increased [Ca2+]cyt and induced secretion. Concomitantly, [Ca2+]cyt increases conducted from the uncaging site induced type 2 cell secretion in both the selected alveolus as well as in neighboring alveoli, indicating the presence of interalveolar communication. These conducted responses were inhibited by pretreating alveoli with the connexin43 (Cx43)-inhibiting peptides gap 26 and gap 27. However, although the conducted [Ca2+]cyt increase diminished with distance from the uncaging site, type 2 cell secretion rates were similar at all locations. We conclude that Cx43-dependent, interalveolar Ca2+ signals regulate type 2 cell secretion in adjacent alveoli. Such interalveolar communication might facilitate acinar coordination of alveolar function.

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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 (February 1, 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 properties of these monolayers were determined in Ussing-type chambers. The addition of 10(-3) M 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) increased the short-circuit current (Isc) from 2.9 +/- 0.75 to 6.9 +/- 0.73 microA/cm2 (means +/- SE; n = 8) and decreased the transepithelial resistance. Cholera toxin, 3-isobutyl-1-methylxanthine, and terbutaline sulfate produced similar increases in Isc and decreases in resistance. The Isc stimulated by 8-BrcAMP was Na but not Cl dependent and could be blocked by amiloride but not by furosemide. Thus 8-BrcAMP and agents that increase intracellular cAMP can stimulate a Na-dependent net active ion transport across alveolar type II cell monolayers. Similar regulatory mechanisms may be involved in controlling solute and fluid movement across the alveolar epithelium in vivo.

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Parra, Saundra C., Ricky Burnette, and Timothy Takaro. "Computer Reconstructions of Normal Human Alveoli From Serial Sections." Proceedings, annual meeting, Electron Microscopy Society of America 43 (August 1985): 312–13. http://dx.doi.org/10.1017/s0424820100118436.

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Portions of two adjacent normal human alveoli were reconstructed from serial sections in order to examine normal alveolar organization, including anatomical relationships among the different cell types, the connective tissue matrix and gaps in the alveolar septum. Computer reconstructions were prepared from montaged electron micrographs of serial sections. Rotation of these reconstructions in the x, y or z axes allowed examination of the alveoli from many different aspects other than the actual plane of sectioning. Anatomical relationships “between Type I and Type II epithelial cells, alveolar macrophages, and pores of Kohn that could not he deduced from a single plane of the section (random sections) were revealed.

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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 (June 1, 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 flattened on fixed fibroblast monolayers and plastic. Alveolar type II cells cultured on plastic released almost all their SP-A into the medium by 4 days. Alveolar type II cells cultured on viable fibroblasts or Matrigel-coated inserts above fibroblasts accumulated SP-A in the medium at a constant rate for the first 4 days, and probably recycle SP-A by endocytosis. The amount of mRNA for SP-A was very low after 4 days of culture of alveolar type II cells on plastic, Matrigel-coated inserts or fixed fibroblast monolayers: relatively, the amount of mRNA for SP-A was increased 4-fold after culture of alveolar type II cells on viable fibroblasts. Co-culture of alveolar type II cells with confluent human dermal fibroblasts stimulated by 2- to 3-fold the secretion of collagen type I into the culture medium, even after the fibroblasts' growth had been arrested with mitomycin C. Collagen secretion, by fibroblasts, also was stimulated 2-fold by conditioned medium from alveolar type II cells cultured on Matrigel. The amount of mRNA for type I collagen increased only modestly when fibroblasts were cultured in this conditioned medium. This stimulation of type I collagen secretion diminished as the conditioned medium was diluted out, but at high dilutions further stimulation occurred, indicating that a factor that inhibited collagen secretion also was being diluted out. The conditioned medium contained low levels of IGF-1 and the stimulation of type I collagen secretion was abolished when the conditioned medium was pre-incubated with antibodies to insulin-like growth factor 1 (IGF-1). There are important reciprocal interactions between alveolar type II cells and fibroblasts in co-culture. Direct contacts between alveolar type II cells and fibroblasts appear to have a trophic effect on cultured alveolar type II cells, increasing the levels of mRNA for SP-A. Rat lung alveolar type II cells appear to release a factor (possibly IGF-1) that stimulates type I collagen secretion by fibroblasts.

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Nicholas, TE. "Control of Turnover of Alveolar Surfactant." Physiology 8, no. 1 (February 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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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 (April 1, 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 levels of podoplanin at postnatal day (pnd)2, and we confirmed by RT-qPCR that these cells are already differentiated but still immature AEC type I. Maturation causes a decrease in isolation yields, reflecting the morphological changes that these cell populations are undergoing. Moreover, we find that major histocompatibility complex II (MHCII), reported as a good marker of AEC type II, is poorly expressed at pnd2 but highly present at pnd8. Combined experiments using LysoTracker and MHCII demonstrate the de novo acquisition of MCHII in AEC type II during lung alveolarization. The lung endothelial populations exhibit FACS signatures from vascular and lymphatic compartments. They can be concomitantly followed throughout alveolar development and were obtained with a noticeable increased yield at the last studied time point (pnd16). Our results provide new insights into early lung alveolar cell isolation feasibility and represent a valuable tool for pure AEC type I preparation as well as further in vitro two- and three-dimensional studies.

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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 (July 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 cells by in situ hybridization and immunohistochemistry of the normal mouse lung; 3) induction of apoptosis in a mouse lung type II epithelial cell line (MLE) after activation of Fas; and 4) induction of apoptosis in a subpopulation of type II cells after the intratracheal instillation of an activating anti-Fas antibody in mice. These findings suggest that Fas-dependent apoptosis is involved in regulating turnover of the alveolar epithelium.

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Chen, Qian, and Yuru Liu. "Heterogeneous groups of alveolar type II cells in lung homeostasis and repair." American Journal of Physiology-Cell Physiology 319, no. 6 (December 1, 2020): C991—C996. http://dx.doi.org/10.1152/ajpcell.00341.2020.

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Alveoli are the gas-exchanging units of the lung, and the alveolar barrier is often a key battleground where pathogens, allergens, and other insults from the environment are encountered. This is seen in the current coronavirus disease 2019 (COVID-19) pandemic, as alveolar epithelium is one of the major targets of SARS-COV-2, the virus that causes COVID-19. Thus, it is essential to understand the mechanisms in order to maintain the integrity of alveoli epithelium. Alveolar type II (AT2) cells behave as tissue stem cells that repair alveoli epithelium during steady-state replacement and after injury. However, not all AT2 cells are equal in their ability for self-renewal or differentiation. Through marker gene identification, lineage tracing, and single-cell RNA-sequencing (scRNA-seq), distinct subpopulations of AT2 cells have been identified that play the progenitor role in a different context. The revelation of AT2 heterogeneity has brought new insights into the role of AT2 cells in various lung disease settings and potentiates the finding of more therapeutics targets. In this mini review, we discuss the recently identified subpopulations of AT2 cells and their functions under steady-state, postinjury, and pathological conditions.

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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 (April 1, 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 membrane gel (Matrigel) or on floating type I collagen gels, expressed markedly less ICAM-1 protein and mRNA compared with cells that had spread on plastic. In contrast, type II cells that had spread as monolayers on dishes coated with basement membrane proteins in planar configuration demonstrated ICAM-1 expression comparable to that of cells on plastic alone. Thus regulation of alveolar epithelial cell expression of this immunologically important adhesion molecule involves complex spatial interactions of the cells with the basement membrane and other epithelial cells.

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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 (December 2007): 699–705. http://dx.doi.org/10.1165/rcmb.2006-0429oc.

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

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Alder, Jonathan K., Christina E. Barkauskas, Nathachit Limjunyawong, Susan E. Stanley, Frant Kembou, Rubin M. Tuder, Brigid L. M. Hogan, Wayne Mitzner, and Mary Armanios. "Telomere dysfunction causes alveolar stem cell failure." Proceedings of the National Academy of Sciences 112, no. 16 (April 3, 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 telomeric repeat-binding factor 2, cells survived but remained dormant and showed all the hallmarks of cellular senescence. Telomere dysfunction in AEC2s triggered an immune response, and this was associated with AEC2-derived up-regulation of cytokine signaling pathways that are known to provoke inflammation in the lung. Mice uniformly died after challenge with bleomycin, underscoring an essential role for telomere function in AEC2s for alveolar repair. Our data show that alveoloar progenitor senescence is sufficient to recapitulate the regenerative defects, inflammatory responses, and susceptibility to injury that are characteristic of telomere-mediated lung disease. They suggest alveolar stem cell failure is a driver of telomere-mediated lung disease and that efforts to reverse it may be clinically beneficial.

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Cao, Chao, Obulkasim Memete, Yiru Shao, Lin Zhang, Fuli Liu, Yu Dun, Daikun He, Jian Zhou, and Jie Shen. "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 (December 23, 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-quality cells were extracted, respectively. All cell types and states were identified and divided into 23 clusters; three cell types were identified: macrophages, epithelial cells, and macrophage proliferating cells. From NC and Gas samples, 1315 and 1756 epithelial cells were extracted, respectively, and divided into 11 clusters. The number of AEC1s decreased considerably following phosgene inhalation. A unique SOX9-positive AEC2 cell type that expanded considerably in the CALI state was identified. This progenitor cell type may develop into alveolar cells, indicating its stem cell differentiation potential. We present a single-cell genome-scale transcription map that can help uncover disease-associated cytologic signatures for understanding biological changes and regeneration of lung tissues during CALI.

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Planus, E., S. Galiacy, M. Matthay, V. Laurent, J. Gavrilovic, G. Murphy, C. Clerici, D. Isabey, C. Lafuma, and M. P. d'Ortho. "Role of collagenase in mediating in vitro alveolar epithelial wound repair." Journal of Cell Science 112, no. 2 (January 15, 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 presence of exogenous collagenases. A similar decrease was observed when cell adhesion was tested on collagen that was first incubated with MMP-1 (versus control on intact collagen). Cell migration on type I collagen was promoted by collagenases. Wound healing of an alveolar epithelial cell monolayer was enhanced in the presence of exogenous collagenases. Our results suggest that collagenases could modulate the repair process by decreasing cell adhesion and cell stiffness, and by increasing cell migration on type I collagen. Collagen degradation could modify cell adhesion sites and collagen degradation peptides could induce alveolar type II pneumocyte migration. New insights regarding alveolar epithelial cell migration are particularly relevant to investigate early events during alveolar epithelial repair following lung injury.

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Massaro, Donald, and Gloria DeCarlo Massaro. "Estrogen receptor regulation of pulmonary alveolar dimensions: alveolar sexual dimorphism in mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 290, no. 5 (May 2006): L866—L870. http://dx.doi.org/10.1152/ajplung.00396.2005.

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Female rats and mice have smaller and, per body mass (BM), more alveoli and alveolar surface area (Sa) than males of their respective species. This sexual dimorphism becomes apparent about the time of sexual maturity. It is prevented in rats (not tested in mice) by ovariectomy at age 3 wk. In female mice, estrogen receptor (ER)-α and ER-β are required for formation of alveoli of appropriate size and number. We now report the average volume of an alveolus (v̄a) and the number of alveoli per body mass (Na/BM) were not statistically different between ER-α−/− and wild type (wt) males. However, the combination of a larger value for v̄a and a smaller value for Na/BM, though neither parameter achieved a statistically significant intergroup difference, resulted in a statistically significant lower Sa/BM in ER-α−/− males compared with wt males. In ER-β−/− males, v̄a was bigger and Na/BM and Sa/BM were lower compared with wt males. Wt males had larger alveoli and lower Na/BM and Sa/BM than wt females. The wt sexual dimorphism of v̄a, Na/BM, and Sa/BM was absent in ER-α−/− mice. Alveolar size did not differ between ER-β−/− females and males but Na/BM and Sa/BM were greater in ER-β−/− females than in ER-β−/− males. The results in male mice, with prior findings in female mice, 1) demonstrate estrogen receptors have a smaller effect on alveolar dimensions in male than female mice, 2) show ER-α and ER-β are required for the sexual dimorphism of alveolar size, and 3) show ER-α is needed for the sexual dimorphism of body mass-specific alveolar number and surface area.

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Housset, B., I. Hurbain, J. Masliah, A. Laghsal, MT Chaumette-Demaugre, H. Karam, and J. Derenne. "Toxic effects of oxygen on cultured alveolar epithelial cells, lung fibroblasts and alveolar macrophages." European Respiratory Journal 4, no. 9 (October 1, 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 fibroblasts and alveolar macrophages isolated from rats. We show that type II cells, when compared with other cell types, are highly sensitive to hyperoxia as shown by increased lactate dehydrogenase (LDH) release, decreased deoxyribose nucleic acid (DNA) and protein content of Petri dishes and decreased thymidine incorporation into DNA. Synthesis of dipalmitoylphosphatidylcholine was also significantly reduced. Antioxidant enzyme activities as well as glutathione content were not higher in type II cells than in other cell types. However, hyperoxia results in a decreased SOD activity and glutathione content in type II cells which was not observed in fibroblasts. We conclude that adaptative changes in SOD and glutathione metabolism could be important defence mechanisms in cells exposed to hyperoxia.

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Kim, H. J., C. A. Henke, S. K. Savik, and D. H. Ingbar. "Integrin mediation of alveolar epithelial cell migration on fibronectin and type I collagen." American Journal of Physiology-Lung Cellular and Molecular Physiology 273, no. 1 (July 1, 1997): L134—L141. http://dx.doi.org/10.1152/ajplung.1997.273.1.l134.

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Acute lung injury leads to type I alveolar epithelial cell (AEC) death, denudation of the alveolar basement membrane, and formation of an alveolar provisional matrix from fibronectin, fibrinogen, and type I collagen. The provisional matrix provides a scaffold for alveolar repair. To restore normal lung architecture, surviving type II AECs must reepithelialize denuded alveoli. We examined whether AECs migrate on provisional matrix proteins and whether integrins mediate this migration using a Boyden chemotaxis chamber. Cultured AECs migrated on fibronectin-coated filters by haptotaxis (defined as movement on a solid-phase substrate) more than one type I collagen-coated filters, and they did not migrate on fibrinogen-coated filters. Soluble fibronectin augmented migration on type I collagen-coated filters, but not on fibronectin-coated filters. Anti-alpha v beta 3-integrin monoclonal antibody (MAb) inhibited migration on substrate-bound fibronectin by 62-77%, whereas anti-beta 1-integrin MAb inhibited migration by 48%. Anti-alpha 2-integrin MAb almost completely inhibited migration on substrate-bound type I collagen, but not on fibronectin. The novel findings in this study are as follows: 1) AECs migrate by haptotaxis more effectively on substrate-bound fibronectin than on type I collagen; 2) alpha v beta 3- and beta 1-integrins partially mediate AEC haptotaxis on fibronectin; and 3) the alpha 2 beta 1-integrin mediates AEC migration on type I collagen. These results support the importance of type II cell migration on provisional matrix proteins during repair of lung injury.

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Downs, Charles A., David W. Montgomery, and Carrie J. Merkle. "Cell culture models using rat primary alveolar type I cells." Pulmonary Pharmacology & Therapeutics 24, no. 5 (October 2011): 577–86. http://dx.doi.org/10.1016/j.pupt.2011.05.005.

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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 (July 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 exocytosis rate correlated with the frequency of [Ca2+]i oscillations. Fluorescence of the lipidophilic dye FM1-43 indicated multiple exocytosis sites per cell. Intracellular Ca2+ chelation and gap junctional inhibition each blocked [Ca2+]i oscillations and exocytosis in type II cells. We demonstrated the feasibility of real-time quantifications in alveolar cells in situ. We conclude that in lung expansion, type II cell exocytosis is modulated by the frequency of intercellularly communicated [Ca2+]i oscillations that are likely to be initiated in type I cells. Thus during lung inflation, type I cells may act as alveolar mechanotransducers that regulate type II cell secretion.

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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 (July 2017): 18–27. http://dx.doi.org/10.1165/rcmb.2016-0426ps.

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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 (July 1, 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 preparations demonstrated decreased viability (by 0.5% trypan blue dye exclusion) when incubated with 50 µM AM for 36 h, and all AM-treated cell preparations demonstrated decreased viability when incubated with 100 or 200 µM AM. Based on a viability index ((viability of AM-treated cells ÷ viability of controls) × 100%), the Clara cell fraction was significantly (p < 0.05) more susceptible than all of the other cell types to 50 µM AM. However, AM cytotoxicity was greatest (p < 0.05) in alveolar macrophages following incubation with 100 or 200 µM AM. There was no difference between any of the enriched cell preparations in the amount of drug accumulated following 24 h of incubation with 50 µM AM, whereas alveolar macrophages accumulated the most drug during incubation with 100 µM AM. Thus, the most susceptible cell type was dependent on AM concentration. AM-induced cytotoxicity in specific cell types may initiate processes leading to inflammation and pulmonary fibrosis.Key words: amiodarone, susceptibility, alveolar macrophage, accumulation.

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Lin, Chih-Ru, Karim Bahmed, and Beata Kosmider. "Impaired Alveolar Re-Epithelialization in Pulmonary Emphysema." Cells 11, no. 13 (June 28, 2022): 2055. http://dx.doi.org/10.3390/cells11132055.

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Alveolar type II (ATII) cells are progenitors in alveoli and can repair the alveolar epithelium after injury. They are intertwined with the microenvironment for alveolar epithelial cell homeostasis and re-epithelialization. A variety of ATII cell niches, transcription factors, mediators, and signaling pathways constitute a specific environment to regulate ATII cell function. Particularly, WNT/β-catenin, YAP/TAZ, NOTCH, TGF-β, and P53 signaling pathways are dynamically involved in ATII cell proliferation and differentiation, although there are still plenty of unknowns regarding the mechanism. However, an imbalance of alveolar cell death and proliferation was observed in patients with pulmonary emphysema, contributing to alveolar wall destruction and impaired gas exchange. Cigarette smoking causes oxidative stress and is the primary cause of this disease development. Aberrant inflammatory and oxidative stress responses result in loss of cell homeostasis and ATII cell dysfunction in emphysema. Here, we discuss the current understanding of alveolar re-epithelialization and altered reparative responses in the pathophysiology of this disease. Current therapeutics and emerging treatments, including cell therapies in clinical trials, are addressed as well.

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Gao, Rui-wei, Xiang-yong Kong, Xiao-xi Zhu, Guo-qing Zhu, Jin-shuai Ma, and Xiu-xiang Liu. "Retinoic acid promotes primary fetal alveolar epithelial type II cell proliferation and differentiation to alveolar epithelial type I cells." In Vitro Cellular & Developmental Biology - Animal 51, no. 5 (December 17, 2014): 479–87. http://dx.doi.org/10.1007/s11626-014-9850-2.

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Fidalgo, Marta F., Catarina G. Fonseca, Paulo Caldas, Alexandre ASF Raposo, Tania Balboni, Lenka Henao-Mišíková, Ana R. Grosso, Francisca F. Vasconcelos, and Cláudio A. Franco. "Aerocyte specification and lung adaptation to breathing is dependent on alternative splicing changes." Life Science Alliance 5, no. 12 (October 11, 2022): e202201554. http://dx.doi.org/10.26508/lsa.202201554.

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Adaptation to breathing is a critical step in lung function and it is crucial for organismal survival. Alveoli are the lung gas exchange units and their development, from late embryonic to early postnatal stages, requires feedbacks between multiple cell types. However, how the crosstalk between the alveolar cell types is modulated to anticipate lung adaptation to breathing is still unclear. Here, we uncovered a synchronous alternative splicing switch in multiple genes in the developing mouse lungs at the transition to birth, and we identified hnRNP A1, Cpeb4, and Elavl2/HuB as putative splicing regulators of this transition. Notably, we found that Vegfa switches from the Vegfa 164 isoform to the longer Vegfa 188 isoform exclusively in lung alveolar epithelial AT1 cells. Functional analysis revealed that VEGFA 188 (and not VEGFA 164) drives the specification of Car4-positive aerocytes, a subtype of alveolar endothelial cells specialized in gas exchanges. Our results reveal that the cell type–specific regulation of Vegfa alternative splicing just before birth modulates the epithelial-endothelial crosstalk in the developing alveoli to promote lung adaptation to breathing.

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Miller, Marian L. "Anatomy of an Alveolar Type II Cell Diagram." Microscopy Today 25, no. 5 (August 31, 2017): 30–35. http://dx.doi.org/10.1017/s1551929517000803.

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Sweeney, Sinbad, Ioannis G. Theodorou, Marta Zambianchi, Shu Chen, Andrew Gow, Stephan Schwander, Junfeng (Jim) Zhang, et al. "Silver nanowire interactions with primary human alveolar type-II epithelial cell secretions: contrasting bioreactivity with human alveolar type-I and type-II epithelial cells." Nanoscale 7, no. 23 (2015): 10398–409. http://dx.doi.org/10.1039/c5nr01496d.

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Tamò, Luca, Youssef Hibaoui, Sampada Kallol, Marco P. Alves, Christiane Albrecht, Katrin E. Hostettler, Anis Feki, 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 (December 1, 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 presence of lamellar bodies, and microvilli, as shown by electron microscopy. Also, LL-iPSC-AEC II expressed AEC type II proteins, such as cytokeratin, surfactant protein C, and LysoTracker DND 26 (a marker for lamellar bodies). Furthermore, the LL-iPSC-AEC II exhibited functional properties of AEC II by an increase of transepithelial electrical resistance over time, secretion of inflammatory mediators in biologically relevant quantities (IL-6 and IL-8), and efficient in vitro alveolar epithelial wound repair. Consistent with the AEC II phenotype, the cell line showed the ability to uptake and release surfactant protein B, to secrete phospholipids, and to differentiate into AEC type I. In summary, we established a long-lasting, but finite AEC type II cell line derived from iPSC as a novel cellular model to study alveolar epithelial cell biology in lung health and disease.

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Herbein, Joel F., Jordan Savov, and Jo Rae Wright. "Binding and uptake of surfactant protein D by freshly isolated rat alveolar type II cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 278, no. 4 (April 1, 2000): L830—L839. http://dx.doi.org/10.1152/ajplung.2000.278.4.l830.

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Alveolar type II cells secrete, internalize, and recycle pulmonary surfactant, a lipid and protein complex that increases alveolar compliance and participates in pulmonary host defense. Surfactant protein (SP) D, a collagenous C-type lectin, has recently been described as a modulator of surfactant homeostasis. Mice lacking SP-D accumulate surfactant in their alveoli and type II cell lamellar bodies, organelles adapted for recycling and secretion of surfactant. The goal of current study was to characterize the interaction of SP-D with rat type II cells. Type II cells bound SP-D in a concentration-, time-, temperature-, and calcium-dependent manner. However, SP-D binding did not alter type II cell surfactant lipid uptake. Type II cells internalized SP-D into lamellar bodies and degraded a fraction of the SP-D pool. Our results also indicated that SP-D binding sites on type II cells may differ from those on alveolar macrophages. We conclude that, in vitro, type II cells bind and recycle SP-D to lamellar bodies, but SP-D may not directly modulate surfactant uptake by type II cells.

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Massaro, Donald, Linda Biadasz Clerch, and Gloria DeCarlo Massaro. "Estrogen receptor-α regulates pulmonary alveolar loss and regeneration in female mice: morphometric and gene expression studies." American Journal of Physiology-Lung Cellular and Molecular Physiology 293, no. 1 (July 2007): L222—L228. http://dx.doi.org/10.1152/ajplung.00384.2006.

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Pulmonary alveoli, especially in females, are estrogen-responsive structures: ovariectomy in wild-type (WT) adult mice results in alveolar loss, and estradiol replacement induces alveolar regeneration. Furthermore, estrogen receptor (ER)-α and ER-β are required for the developmental formation of a full complement of alveoli in female mice. We now show ovariectomy resulted in alveolar loss in adult ER-β−/− mice but not in adult ER-α−/− mice. Estradiol treatment of ovariectomized ER-β−/− mice induced alveolar regeneration. In ovariectomized WT mice, estradiol treatment resulted, within 1 h, in RNA-level gene expression supportive of processes needed to form an alveolar septum, e.g., cell replication, angiogenesis, extracellular matrix remodeling, and guided cell motion. Among these processes, protein expression supporting angiogenesis and cell replication was elevated 1 and 3 h, respectively, after estradiol treatment; similar findings were not present in either mutant. We conclude: 1) loss of signaling via ER-β is not required for postovariectomy-induced alveolar loss or estradiol-induced regeneration; this indicates ER-α is key for estrogen-related alveolar loss and regeneration in adult female mice; 2) taken together with prior work showing that developmental formation of a full complement of alveoli requires ER-α and ER-β, the present findings indicate the developmental and regenerative formation of alveoli are regulated differently, i.e., signaling for alveolar regeneration is not merely a recapitulation of signaling for developmental alveologenesis; and 3) the timing of estradiol-induced gene expression in lung supportive of processes required to form a septum differs between ovariectomized WT and ER-β−/− mice.

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Dobbs, L. G. "Isolation and culture of alveolar type II cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 258, no. 4 (April 1, 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 addresses many of the issues involved in isolating and culturing type II cells, including the choice of a method of isolating cells, the importance of using specific markers of the differentiated type II cell phenotype, and the problems of maintaining these differentiated phenotypic characteristics in tissue culture.

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Foster, Cherie D., Linda S. Varghese, Linda W. Gonzales, Susan S. Margulies, and Susan H. Guttentag. "The Rho Pathway Mediates Transition to an Alveolar Type I Cell Phenotype During Static Stretch of Alveolar Type II Cells." Pediatric Research 67, no. 6 (June 2010): 585–90. http://dx.doi.org/10.1203/pdr.0b013e3181dbc708.

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39

Saari, Seppo A. m. "Different Cell Types In the Lower Respiratory Tract of the Reindeer (Rangifer tarandus tarandus L.) - A Transmission Electron Microscopical Study." Rangifer 17, no. 2 (February 1, 1997): 73. http://dx.doi.org/10.7557/2.17.2.1304.

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The epithelium of the trachea and distal airways of 12 healthy adult reindeer were studied with transmission electron microscopy. The ultrastructure of the reindeer respiratory tract corresponded to the findings of previous investigators studying other mammalian species. The epithelium of the trachea and bronchi, down to the level of the distal bronchioli, was composed of three main types of cell: ciliated, goblet, and basal. In the distal brochioli, non-ciliated cells similar to those known as Clara cells were predominant. Numerous electron-dense granules and the cell organelle pattern resembled the Clara cell type observed in laboratory rodents, rabbit, sheep, pig, horse, and llama. Pneumocyte 1 and pneumocyte 2 cells were readily identified in the alveoli. The pneumocyte 2 cells possessed short microvilli and granules with lamellar content. Micropinocytotic vesicles were very numerous in the alveolar wall, and a small number of alveolar macrophages occasionally seen in the alveolar lumen.

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Hou, Wen-Li, Ming Chang, Xiao-Feng Liu, Lin-Sen Hu, and Shu-Cheng Hua. "Proteomic and ultrastructural analysis of Clara cell and type II alveolar epithelial cell-type lung cancer cells." Translational Cancer Research 9, no. 2 (February 2020): 565–76. http://dx.doi.org/10.21037/tcr.2019.12.04.

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Tan, Ju Jing, Francis Boudreault, Damien Adam, Emmanuelle Brochiero, and Ryszard Grygorczyk. "Type 2 secretory cells are primary source of ATP release in mechanically stretched lung alveolar cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 318, no. 1 (January 1, 2020): L49—L58. http://dx.doi.org/10.1152/ajplung.00321.2019.

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Extracellular ATP and its metabolites are potent paracrine modulators of lung alveolar cell function, including surfactant secretion and fluid transport, but the sources and mechanism of intra-alveolar ATP release remain unclear. To determine the contribution of gas-exchanging alveolar type 1 (AT1) and surfactant-secreting type 2 (AT2) cells to stretch-induced ATP release, we used quantitative real-time luminescence ATP imaging and rat primary alveolar cells cultured on silicon substrate for 2–7 days. When cultured on solid support, primary AT2 cells progressively transdifferentiated into AT1-like cells with ~20% of cells showing AT1 phenotype by day 2–3 (AT2:AT1 ≈ 4:1), while on day 7, the AT2:AT1 cell ratio was reversed with up to 80% of the cells displaying characteristics of AT1 cells. Stretch (1 s, 5–35%) induced ATP release from AT2/AT1 cell cultures, and it was highest on days 2 and 3 but declined in older cultures. ATP release tightly correlated with the number of remaining AT2 cells in culture, consistent with ~10-fold lower ATP release by AT1 than AT2 cells. ATP release was unaffected by inhibitors of putative ATP channels carbenoxolone and probenecid but was significantly diminished in cells loaded with calcium chelator BAPTA. These pharmacological modulators had similar effects on stretch-induced intracellular Ca2+ responses measured by Fura2 fluorescence. The study revealed that AT2 cells are the primary source of stretch-induced ATP release in heterocellular AT2/AT1 cell cultures, suggesting similar contribution in intact alveoli. Our results support a role for calcium-regulated mechanism but not ATP-conducting channels in ATP release by alveolar epithelial cells.

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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 (January 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 cell (≥ 12 μm) number also increased at 16 weeks of age (P < 0.06). Accompanying the increases in cell size and number was an increase in alveolar wall area (25.6%, or 21.4% with the type 2 cell field area excluded). Since the wall area increase was less than that for type 2 cell field area or type 2 cell mean area but greater than the type 2 cell number increase, there were disparate trends in the ratios comparing cell area and cell number to alveolar wall area. Significantly, type 2 cell numbers, mean type 2 cell area, and alveolar wall area had not plateaued at 16 weeks of age. Thus, there is the implication that the type 2 cell population and the alveolar walls are still undergoing changes at least up to the age of 10 weeks and possibly beyond 16 weeks of age. This is a longer period of lung development than expected from prior literature reports and raises the question of a correspondingly greater period of increased susceptibility to noxious air pollutants. An influence of an ambient level of NO2 exposure on the developing mouse lung is the subject of Part II of this investigation.

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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 (February 2016): 30–36. http://dx.doi.org/10.1089/cell.2015.0015.

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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 (February 1, 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 cells and increased permeability of the alveolar epithelium to protein tracers. In contrast, the lactate dehydrogenase activity of alveolar fluid from PA103-treated rats was elevated only threefold over control values at 6 h (P < 0.05). In a second study using a less injurious strain of P. aeruginosa (PA103 exsA::omega), the alveolar fluid content of rTI40 was the same as control values. These findings indicate that the alveolar fluid content of a type I cell-specific protein can be used as a sensitive and specific biochemical marker of type I cell injury.

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Lee, Vivian Y., Clara Schroedl, Joslyn K. Brunelle, Leonard J. Buccellato, Ozkan I. Akinci, Hideaki Kaneto, Colleen Snyder, James Eisenbart, G. R. Scott Budinger, and Navdeep S. Chandel. "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 (October 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 not undergo cell death in response to bleomycin. Dominant negative Fas-associating protein with a death domain failed to prevent bleomycin-induced cell death in MLE-12 cells. Caspase-8 inhibitor CrmA did not prevent bleomycin-induced cell death in primary rat alveolar type II cells. Furthermore, fibroblast cells deficient in Bax and Bak, but not Bid, were resistant to bleomycin-induced cell death. To determine whether the stress kinase JNK was an upstream regulator of Bax activation, MLE-12 cells were exposed to bleomycin in the presence of an adenovirus encoding a dominant negative JNK. Bleomycin-induced Bax activation was prevented by the expression of a dominant negative JNK in MLE-12 cells. Dominant negative JNK prevented cell death in MLE-12 cells and in primary rat alveolar type II cells exposed to bleomycin. These data indicate that bleomycin induces cell death through a JNK-dependent mitochondrial death pathway in alveolar epithelial cells.

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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 (August 1, 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 blocked this adhesion. Flow cytometry and Western analysis indicated that type II cells expressed beta 1- and alpha v beta 3-integrins. Anti-beta 1-and anti-alpha v beta 3-integrin antibodies blocked type II cell adhesion to fibronectin and to fibronectin and fibrinogen, respectively. In summary, type II cells adhered to fibronectin, fibrinogen, and fibrin, and adhesion was partially mediated by integrins. This study provides the first evidence of type II cell adhesion to fibrin gels and vitronectin, beta 1- and alpha v beta 3-integrin mediation of type II cell adhesion, and the presence of the alpha v beta 3-integrin on type II epithelial cells.

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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 (April 2004): 500–509. http://dx.doi.org/10.1165/rcmb.4890.

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Seitz, Daniel H., Mario Perl, Stefanie Mangold, Anne Neddermann, Sonja T. Braumüller, Shaoixa Zhou, Max G. Bachem, Markus S. Huber-Lang, and Markus W. Knöferl. "PULMONARY CONTUSION INDUCES ALVEOLAR TYPE 2 EPITHELIAL CELL APOPTOSIS." Shock 30, no. 5 (November 2008): 537–44. http://dx.doi.org/10.1097/shk.0b013e31816a394b.

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Sanchez-Esteban, Juan, Lawrence A. Cicchiello, Yulian Wang, Shu-Whei Tsai, Lakisha K. Williams, John S. Torday, and Lewis P. Rubin. "Mechanical stretch promotes alveolar epithelial type II cell differentiation." Journal of Applied Physiology 91, no. 2 (August 1, 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 increased surfactant protein (SP) C mRNA expression by 150 ± 30% over controls ( P < 0.02) on gestational day 18 and by 130 ± 30% on day 19 ( P< 0.03). Stretch of cocultures with fibroblasts increased SP-C expression on days 18 and 19 by 170 ± 40 and 270 ± 40%, respectively, compared with unstretched cocultures. On day 19, stretch of isolated type II cells increased SP-B mRNA expression by 50% ( P < 0.003). Unlike SP-C, addition of fibroblasts did not produce significant additional effects on SP-B mRNA levels. Under these conditions, we observed only modest increases in cellular immunoreactive SP-B, but secreted saturated phosphatidylcholine rose by 40% ( P< 0.002). These results indicate that cyclic stretch promotes developmentally timed differentiation of fetal type II cells, as a direct effect on epithelial cell function and via mesenchymal-epithelial interactions. Expression of the SP-C gene appears to be highly responsive to mechanical stimulation.

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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 (January 1994): 1229–35. http://dx.doi.org/10.1016/0024-3205(94)00662-8.

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Journal articles on the topic 'Alveolar type cell'

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