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Journal articles on the topic 'Lung alveolar cells'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Zhang, Honglei, Yong Cui, Zhiyu Zhou, Yan Ding, and Hongguang Nie. "Alveolar Type 2 Epithelial Cells as Potential Therapeutics for Acute Lung Injury/Acute Respiratory Distress Syndrome." Current Pharmaceutical Design 25, no. 46 (2020): 4877–82. http://dx.doi.org/10.2174/1381612825666191204092456.

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: Acute lung injury/acute respiratory distress syndrome is a common clinical illness with high morbidity and mortality, which is still one of the medical problems urgently needed to be solved. Alveolar type 2 epithelial cells are an important component of lung epithelial cells and as a kind of stem cells, they can proliferate and differentiate into alveolar type 1 epithelial cells, thus contributing to lung epithelial repairment. In addition, they synthesize and secrete all components of the surfactant that regulates alveolar surface tension in the lungs. Moreover, alveolar type 2 epithelial c

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2

Wu, Huijuan, and Nan Tang. "Stem cells in pulmonary alveolar regeneration." Development 148, no. 2 (2021): dev193458. http://dx.doi.org/10.1242/dev.193458.

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ABSTRACTThe lungs are constantly exposed to the external environment and are therefore vulnerable to insults that can cause infection and injury. Maintaining the integrity and barrier function of the lung epithelium requires complex interactions of multiple cell lineages. Elucidating the cellular players and their regulation mechanisms provides fundamental information to deepen understanding about the responses and contributions of lung stem cells. This Review focuses on advances in our understanding of mammalian alveolar epithelial stem cell subpopulations and discusses insights about the reg

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Herrero, Raquel, Mishie Tanino, Lincoln S. Smith, et al. "The Fas/FasL pathway impairs the alveolar fluid clearance in mouse lungs." American Journal of Physiology-Lung Cellular and Molecular Physiology 305, no. 5 (2013): L377—L388. http://dx.doi.org/10.1152/ajplung.00271.2012.

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Alveolar epithelial damage is a critical event that leads to protein-rich edema in acute lung injury (ALI), but the mechanisms leading to epithelial damage are not completely understood. Cell death by necrosis and apoptosis occurs in alveolar epithelial cells in the lungs of patients with ALI. Fas activation induces apoptosis of alveolar epithelial cells, but its role in the formation of lung edema is unclear. The main goal of this study was to determine whether activation of the Fas/Fas ligand pathway in the lungs could alter the function of the lung epithelium, and the mechanisms involved. T

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Rakhmonova, H.N, S.M Mukhitdinova, and F.Z Rakhmonov. "MORPHOLOGICAL STRUCTURE OF NEUROEPITHELIAL CELLS IN RABBIT LUNGS." Journal of Science-Innovative Research in Uzbekistan 2, no. 2 (2024): 153–56. https://doi.org/10.5281/zenodo.10645714.

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The morphofunctional features of NET in the developing respiratory lung have been studied. Lungs of 23 rabbits aged 1-30 days served as a material for the study. Paraffin sections were stained with hematoxylin and eosin, according to the Van-Gizon method, impregnated according to the Grimelius method. Histochemical detection of acetylcholinesterase (AChE) activity was carried out on frozen sections of unfixed lungs by the method of M. Karnovsky and L. Roots. The study allowed to establish that in the rabbit lung NET cells are detected in the respiratory secti

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Khalil, N., R. N. O'Connor, K. C. Flanders, W. Shing, and C. I. Whitman. "Regulation of type II alveolar epithelial cell proliferation by TGF-beta during bleomycin-induced lung injury in rats." American Journal of Physiology-Lung Cellular and Molecular Physiology 267, no. 5 (1994): L498—L507. http://dx.doi.org/10.1152/ajplung.1994.267.5.l498.

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Three isoforms of transforming growth factor-beta (TGF-beta) are found in mammalian cells and are potent regulators of inflammation, connective tissue synthesis, cellular proliferation, and differentiation. To determine the distribution and regulation of TGF-beta isoforms during pulmonary injury, a rat model of bleomycin-induced lung inflammation and repair was used. Using immunohistochemistry, we demonstrate that TGF-beta 2 and TGF-beta 3 were localized to alveolar macrophages as well as epithelial and smooth muscle cells of both normal rat lungs and rat lungs obtained at all time intervals a

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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

Lindahl, P., L. Karlsson, M. Hellstrom, et al. "Alveogenesis failure in PDGF-A-deficient mice is coupled to lack of distal spreading of alveolar smooth muscle cell progenitors during lung development." Development 124, no. 20 (1997): 3943–53. http://dx.doi.org/10.1242/dev.124.20.3943.

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PDGF-A(−/−) mice lack lung alveolar smooth muscle cells (SMC), exhibit reduced deposition of elastin fibres in the lung parenchyma, and develop lung emphysema due to complete failure of alveogenesis. We have mapped the expression of PDGF-A, PDGF receptor-alpha, tropoelastin, smooth muscle alpha-actin and desmin in developing lungs from wild type and PDGF-A(−/−) mice of pre- and postnatal ages in order to get insight into the mechanisms of PDGF-A-induced alveolar SMC formation and elastin deposition. PDGF-A was expressed by developing lung epithelium. Clusters of PDGF-Ralpha-positive (PDGF-Ralp

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8

Wu, Ailing, and Hai Song. "Regulation of alveolar type 2 stem/progenitor cells in lung injury and regeneration." Acta Biochimica et Biophysica Sinica 52, no. 7 (2020): 716–22. http://dx.doi.org/10.1093/abbs/gmaa052.

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Abstract The renewal of lung epithelial cells is normally slow unless the lung is injured. The resident epithelial stem cells rapidly proliferate and differentiate to maintain lung structure and function when the lung is damaged. The alveolar epithelium is characterized by alveolar type 1 (AT1) and alveolar type 2 (AT2) cells. AT2 cells are the stem cells for alveoli, as they can both self-renew and generate AT1 cells. Abnormal proliferation and regulation of AT2 cells will lead to serious lung diseases including cancers. In this review, we focused on the alveolar stem/progenitor cells, the ke

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9

Wodopia, Ralf, Hyun Soo Ko, Javiera Billian, Rudolf Wiesner, Peter Bärtsch, and Heimo Mairbäurl. "Hypoxia decreases proteins involved in epithelial electrolyte transport in A549 cells and rat lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 6 (2000): L1110—L1119. http://dx.doi.org/10.1152/ajplung.2000.279.6.l1110.

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Fluid reabsorption from alveolar space is driven by active Na reabsorption via epithelial Na channels (ENaCs) and Na-K-ATPase. Both are inhibited by hypoxia. Here we tested whether hypoxia decreases Na transport by decreasing the number of copies of transporters in alveolar epithelial cells and in lungs of hypoxic rats. Membrane fractions were prepared from A549 cells exposed to hypoxia (3% O2) as well as from whole lung tissue and alveolar type II cells from rats exposed to hypoxia. Transport proteins were measured by Western blot analysis. In A549 cells, α1- and β1-Na-K-ATPase, Na/K/2Cl cotr

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10

Hastings, Randolph H., John T. Berg, Daphne Summers-Torres, Douglas W. Burton, and Leonard J. Deftos. "Parathyroid hormone-related protein reduces alveolar epithelial cell proliferation during lung injury in rats." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 1 (2000): L194—L200. http://dx.doi.org/10.1152/ajplung.2000.279.1.l194.

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Parathyroid hormone-related protein (PTHrP) is a growth inhibitor for alveolar type II cells and could be a regulatory factor for alveolar epithelial cell proliferation after lung injury. We investigated lung PTHrP expression in rats exposed to 85% oxygen. Lung levels of PTHrP were significantly decreased between 4 and 8 days of hyperoxia, concurrent with increased expression of proliferating cell nuclear antigen and increased incorporation of 5-bromo-2′-deoxyuridine (BrdU) into DNA in lung corner cells. PTHrP receptor was present in both normal and hyperoxic lung. To test whether the fall in

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Matute-Bello, Gustavo, W. Conrad Liles, Charles W. Frevert, et al. "Recombinant human Fas ligand induces alveolar epithelial cell apoptosis and lung injury in rabbits." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 2 (2001): L328—L335. http://dx.doi.org/10.1152/ajplung.2001.281.2.l328.

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This study investigated whether recombinant human soluble Fas ligand (rh-sFasL) induces apoptosis of primary type II pneumocytes in vitro and lung injury in vivo. Type II cells isolated from normal rabbit lung expressed Fas on their surface and became apoptotic after an 18-h incubation with rh-sFasL. Fas expression in normal rabbit lungs was localized by immunohistochemistry to alveolar and airway epithelia and alveolar macrophages. The administration of 10 μg of rh-sFasL into the right lungs of rabbits resulted 24 h later in both significantly more bronchoalveolar lavage fluid total protein a

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Misharin, Alexander V., Luisa Morales-Nebreda, Paul A. Reyfman, et al. "Monocyte-derived alveolar macrophages drive lung fibrosis and persist in the lung over the life span." Journal of Experimental Medicine 214, no. 8 (2017): 2387–404. http://dx.doi.org/10.1084/jem.20162152.

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Little is known about the relative importance of monocyte and tissue-resident macrophages in the development of lung fibrosis. We show that specific genetic deletion of monocyte-derived alveolar macrophages after their recruitment to the lung ameliorated lung fibrosis, whereas tissue-resident alveolar macrophages did not contribute to fibrosis. Using transcriptomic profiling of flow-sorted cells, we found that monocyte to alveolar macrophage differentiation unfolds continuously over the course of fibrosis and its resolution. During the fibrotic phase, monocyte-derived alveolar macrophages diff

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Rojas, Joselyn Joanna, Francesca Polverino, Xiaoyan Gai, et al. "Adam8 limits emphysema development in smoke-exposed mice: A new player in the pathogenesis of COPD." Journal of Immunology 198, no. 1_Supplement (2017): 55.38. http://dx.doi.org/10.4049/jimmunol.198.supp.55.38.

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Abstract Background A disintegrin and metalloproteinase-8 (ADAM8) is expressed by lung cells implicated COPD pathogenesis. It’s not known whether ADAM8 contributes to COPD pathogenesis. Methods ADAM8 expression was measured in the lungs of COPD patients and controls, and mice exposed to cigarette smoke (CS) versus air by staining lung sections for ADAM8 and markers of different lung cells. Emphysema development and small airway fibrosis were evaluated wild-type (WT), Adam8−/− and Adam8 bone marrow chimeric mice exposed to air or CS for 6 months. Lung inflammation, alveolar septal cell apoptosi

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Kemp, Paul J., and Kwang-Jin Kim. "Spectrum of ion channels in alveolar epithelial cells: implications for alveolar fluid balance." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 3 (2004): L460—L464. http://dx.doi.org/10.1152/ajplung.00191.2004.

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The efficient transition from placental to atmospheric delivery of oxygen at birth is critically dependent on rapid reabsorption of fetal lung fluid. In the perinatal period, this process is driven by active transepithelial sodium transport and is almost exclusively dependent on expression and modulation of the amiloride-sensitive epithelial sodium channel (ENaC). However, later in development, the amiloride sensitivity of the reabsorptive response, which must be sustained to keep the lungs effectively dry, wanes as a function of postnatal age. This Featured Topic (Experimental Biology Meeting

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Rotin, D., B. J. Goldstein, and C. A. Fladd. "Expression of the tyrosine phosphatase LAR-PTP2 is developmentally regulated in lung epithelia." American Journal of Physiology-Lung Cellular and Molecular Physiology 267, no. 3 (1994): L263—L270. http://dx.doi.org/10.1152/ajplung.1994.267.3.l263.

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The role of tyrosine kinases in regulating cell proliferation, differentiation, and development has been well documented. In contrast, little is known about the role of protein tyrosine phosphatases (PTPs) in mammalian development. To identify PTPs that may be involved in lung development, we have isolated (by polymerase chain reaction) from rat fetal alveolar epithelial cells a cDNA fragment which was identified as the recently cloned tyrosine phosphatase LAR-PTP2. Analysis of tissue expression of LAR-PTP2 identified a approximately 7.5-kb message in the lung, which is also expressed weakly i

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Bem, R. A., A. W. Farnand, V. Wong, et al. "Depletion of resident alveolar macrophages does not prevent Fas-mediated lung injury in mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 295, no. 2 (2008): L314—L325. http://dx.doi.org/10.1152/ajplung.00210.2007.

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Activation of the Fas/Fas ligand (FasL) system in the lungs results in a form of injury characterized by alveolar epithelial apoptosis and neutrophilic inflammation. Studies in vitro show that Fas activation induces apoptosis in alveolar epithelial cells and cytokine production in alveolar macrophages. The main goal of this study was to determine the contribution of alveolar macrophages to Fas-induced lung inflammation in mice, by depleting alveolar macrophages using clodronate-containing liposomes. Liposomes containing clodronate or PBS were instilled by intratracheal instillation. After 24 h

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Rider, E. D., M. Ikegami, and A. H. Jobe. "Localization of alveolar surfactant clearance in rabbit lung cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 263, no. 2 (1992): L201—L209. http://dx.doi.org/10.1152/ajplung.1992.263.2.l201.

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Localization of surfactant phospholipid clearance in lung cells was investigated in vivo in rabbits using radiolabeled dipalmitoylphosphatidylcholine (DPPC) and 1,2-dihexa-decyl-sn-glycero-3-phosphocholine (DPPC-ether), a phospholipase A1- and A2-resistant analogue of DPPC. After intratracheal injection of liposomes of the labeled lipids associated with unlabeled surfactant, adult rabbits were killed in groups of three to five at 0, 4, 12, and 24 h with recovery of bronchoalveolar lavages for alveolar macrophages and surfactant. Type II cells and tissue-associated macrophages were isolated on

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18

Sznajder, Jacob I., Karen M. Ridge, Donovan B. Yeates, John Ilekis, and Walter Olivera. "Epidermal growth factor increases lung liquid clearance in rat lungs." Journal of Applied Physiology 85, no. 3 (1998): 1004–10. http://dx.doi.org/10.1152/jappl.1998.85.3.1004.

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Epidermal growth factor (EGF) has been reported to stimulate the proliferation of epithelial cells and increase Na+flux and Na+-K+-ATPase function in alveolar epithelial cell monolayers. Increases in Na+-K+-ATPase in alveolar type II cells (AT2) have been associated with increased active Na+ transport and lung edema clearance across the rat alveolar epithelium in a model of proliferative lung injury. Thus we tested whether administration of aerosolized EGF to rat lungs would increase active Na+ transport and lung liquid clearance. Sixteen adult Sprague-Dawley male rats were randomized to three

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Wirsching, Eva, Michael Fauler, Giorgio Fois, and Manfred Frick. "P2 Purinergic Signaling in the Distal Lung in Health and Disease." International Journal of Molecular Sciences 21, no. 14 (2020): 4973. http://dx.doi.org/10.3390/ijms21144973.

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The distal lung provides an intricate structure for gas exchange in mammalian lungs. Efficient gas exchange depends on the functional integrity of lung alveoli. The cells in the alveolar tissue serve various functions to maintain alveolar structure, integrity and homeostasis. Alveolar epithelial cells secrete pulmonary surfactant, regulate the alveolar surface liquid (ASL) volume and, together with resident and infiltrating immune cells, provide a powerful host-defense system against a multitude of particles, microbes and toxicants. It is well established that all of these cells express purine

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Saldías, F. J., A. P. Comellas, L. Pesce, E. Lecuona, and J. I. Sznajder. "Dopamine increases lung liquid clearance during mechanical ventilation." American Journal of Physiology-Lung Cellular and Molecular Physiology 283, no. 1 (2002): L136—L143. http://dx.doi.org/10.1152/ajplung.00089.2000.

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Short-term mechanical ventilation with high tidal volume (HVT) causes mild to moderate lung injury and impairs active Na+ transport and lung liquid clearance in rats. Dopamine (DA) enhances active Na+ transport in normal rat lungs by increasing Na+-K+-ATPase activity in the alveolar epithelium. We examined whether DA would increase alveolar fluid reabsorption in rats ventilated with HVT for 40 min compared with those ventilated with low tidal volume (LVT) and with nonventilated rats. Similar to previous reports, HVT ventilation decreased alveolar fluid reabsorption by ∼50% ( P < 0.001). DA

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Nova, Zuzana, Henrieta Skovierova, and Andrea Calkovska. "Alveolar-Capillary Membrane-Related Pulmonary Cells as a Target in Endotoxin-Induced Acute Lung Injury." International Journal of Molecular Sciences 20, no. 4 (2019): 831. http://dx.doi.org/10.3390/ijms20040831.

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The main function of the lungs is oxygen transport from the atmosphere into the blood circulation, while it is necessary to keep the pulmonary tissue relatively free of pathogens. This is a difficult task because the respiratory system is constantly exposed to harmful substances entering the lungs by inhalation or via the blood stream. Individual types of lung cells are equipped with the mechanisms that maintain pulmonary homeostasis. Because of the clinical significance of acute respiratory distress syndrome (ARDS) the article refers to the physiological role of alveolar epithelial cells type

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Gazdhar, Amiq, Patrick Fachinger, Coretta van Leer, et al. "Gene transfer of hepatocyte growth factor by electroporation reduces bleomycin-induced lung fibrosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 292, no. 2 (2007): L529—L536. http://dx.doi.org/10.1152/ajplung.00082.2006.

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Abnormal alveolar wound repair contributes to the development of pulmonary fibrosis after lung injury. Hepatocyte growth factor (HGF) is a potent mitogenic factor for alveolar epithelial cells and may therefore improve alveolar epithelial repair in vitro and in vivo. We hypothesized that HGF could increase alveolar epithelial repair in vitro and improve pulmonary fibrosis in vivo. Alveolar wound repair in vitro was determined using an epithelial wound repair model with HGF-transfected A549 alveolar epithelial cells. Electroporation-mediated, nonviral gene transfer of HGF in vivo was performed

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Blagojević, Miloš, Ivana Božičković, Gordana Ušćebrka, et al. "Anatomical and histological characteristics of the lungs in the ground squirrel (Spermophilus citellus)." Acta Veterinaria Hungarica 66, no. 2 (2018): 165–76. http://dx.doi.org/10.1556/004.2018.016.

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The aim of this work was to study the topography, morphology, vascularisation, histology and innervation of the lungs in the ground squirrel (Spermophilus citellus) and compare these data with those concerning the rat, mole rat, rabbit and mouse. The research was carried out on 15 animals. It was revealed that the right lung has four lobes (cranial, middle, caudal and accessory lobes), while the left lung is not divided into segments. The functional vessels are a. pulmonalis dextra et sinistra and vv. pulmonales (5–6), while the nutritive vessels of the lungs are a. bronchoesophagea dextra and

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Gokey, Jason J., John Snowball, Jenna Green, et al. "Pretreatment of aged mice with retinoic acid supports alveolar regeneration via upregulation of reciprocal PDGFA signalling." Thorax 76, no. 5 (2021): 456–67. http://dx.doi.org/10.1136/thoraxjnl-2020-214986.

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ObjectivesIdiopathic pulmonary fibrosis (IPF) primarily affects the aged population and is characterised by failure of alveolar regeneration, leading to loss of alveolar type 1 (AT1) cells. Aged mouse models of lung repair have demonstrated that regeneration fails with increased age. Mouse and rat lung repair models have shown retinoic acid (RA) treatment can restore alveolar regeneration. Herein, we seek to determine the signalling mechanisms that become activated on RA treatment prior to injury, which support alveolar differentiation.DesignPartial pneumonectomy lung injury model and next-gen

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Ahmadvand, Negah, Gianni Carraro, Matthew R. Jones, et al. "Cell-Surface Programmed Death Ligand-1 Expression Identifies a Sub-Population of Distal Epithelial Cells Enriched in Idiopathic Pulmonary Fibrosis." Cells 11, no. 10 (2022): 1593. http://dx.doi.org/10.3390/cells11101593.

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Idiopathic lung fibrosis (IPF) is a fatal lung disease characterized by chronic epithelial injury and exhausted repair capacity of the alveolar compartment, associated with the expansion of cells with intermediate alveolar epithelial cell (AT2) characteristics. Using SftpcCreERT2/+: tdTomatoflox/flox mice, we previously identified a lung population of quiescent injury-activated alveolar epithelial progenitors (IAAPs), marked by low expression of the AT2 lineage trace marker tdTomato (Tomlow) and characterized by high levels of Pd-l1 (Cd274) expression. This led us to hypothesize that a populat

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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 (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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Tschumperlin, Daniel J., and Susan S. Margulies. "Alveolar epithelial surface area-volume relationship in isolated rat lungs." Journal of Applied Physiology 86, no. 6 (1999): 2026–33. http://dx.doi.org/10.1152/jappl.1999.86.6.2026.

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In vitro studies of the alveolar epithelial response to deformation require knowledge of the in situ mechanical environment of these cells. Because of the presence of tissue folding and crumpling, previous measurements of the alveolar surface area available for gas exchange are not equivalent to the epithelial surface area. To identify epithelial deformations in uniformly inflated lungs representative of the in vivo condition, we studied isolated Sprague-Dawley rat lungs ( n = 31) fixed by perfusion with glutaraldehyde on deflation after cycling three times at high lung volume (10–25 cmH2O). T

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Kramer, Boris W., Susanne Kramer, Machiko Ikegami, and Alan H. Jobe. "Injury, inflammation, and remodeling in fetal sheep lung after intra-amniotic endotoxin." American Journal of Physiology-Lung Cellular and Molecular Physiology 283, no. 2 (2002): L452—L459. http://dx.doi.org/10.1152/ajplung.00407.2001.

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Chorioamnionitis is frequent in preterm labor and increases the risk of bronchopulmonary dysplasia. We hypothesized that intra-amniotic endotoxin injures the lung in utero, causing a sequence of inflammation and tissue injury similar to that which occurs in the injured adult lung. Preterm lamb lungs at 125 days gestational age were evaluated for indicators of inflammation, injury, and repair 5 h, 24 h, 72 h, and 7 days after 4 mg of intra-amniotic endotoxin injection. At 5 h, the epithelial cells in large airways expressed heat shock protein 70, and alveolar interleukin-8 was increased. Surfac

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Kida, Hiroshi, Mitsuhiro Yoshida, Shigenori Hoshino, et al. "Protective effect of IL-6 on alveolar epithelial cell death induced by hydrogen peroxide." American Journal of Physiology-Lung Cellular and Molecular Physiology 288, no. 2 (2005): L342—L349. http://dx.doi.org/10.1152/ajplung.00016.2004.

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The goal of this study was to examine whether IL-6 could directly protect lung resident cells, especially alveolar epithelial cells, from reactive oxygen species (ROS)-induced cell death. ROS induced IL-6 gene expression in organotypic lung slices of wild-type (WT) mice. ROS also induced IL-6 gene expression in mouse primary lung fibroblasts, dose dependently. The organotypic lung slices of WT were more resistant to ROS-induced DNA fragmentation than those of IL-6-deficient (IL-6−/−) mice. WT resistance against ROS was abrogated by treatment with anti-IL-6 antibody. TdT-mediated dUTP nick end

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Nabors, L. Karina, William A. Baumgartner, Steven J. Janke, James R. Rose, Wiltz W. Wagner, and Ronald L. Capen. "Red blood cell orientation in pulmonary capillaries and its effect on gas diffusion." Journal of Applied Physiology 94, no. 4 (2003): 1634–40. http://dx.doi.org/10.1152/japplphysiol.01021.2001.

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When alveoli are inflated, the stretched alveolar walls draw their capillaries into oval cross sections. This causes the disk-shaped red blood cells to be oriented near alveolar gas, thereby minimizing diffusion distance. We tested these ideas by measuring red blood cell orientation in histological slides from rapidly frozen rat lungs. High lung inflation did cause the capillaries to have oval cross sections, which constrained the red blood cells within them to flow with their broad sides facing alveolar gas. Low lung inflation stretched alveolar walls less and allowed the capillaries to assum

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Saito, Satoshi, Jun-ichi Ogawa, and Yoshihiro Minamiya. "Pulmonary reexpansion causes xanthine oxidase-induced apoptosis in rat lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 3 (2005): L400—L406. http://dx.doi.org/10.1152/ajplung.00136.2005.

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The pathogenesis of reexpansion pulmonary edema is not yet fully understood. We therefore studied its mechanism in a rat model in which the left lung was collapsed by bronchial occlusion for 1 h and then reexpanded and ventilated for an additional 3 h. We then evaluated the production of reactive oxygen species in the lungs using fluorescent imaging and cerium deposition electron microscopic techniques and the incidence of apoptosis using the TdT-mediated dUTP-digoxigenin nick end labeling (TUNEL) method. We found that pulmonary reexpansion induced production of reactive oxygen species and the

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Swystun, Veronica, Lan Chen, Phillip Factor, Brian Siroky, P. Darwin Bell, and Sadis Matalon. "Apical trypsin increases ion transport and resistance by a phospholipase C-dependent rise of Ca2+." American Journal of Physiology-Lung Cellular and Molecular Physiology 288, no. 5 (2005): L820—L830. http://dx.doi.org/10.1152/ajplung.00396.2004.

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We investigated the mechanisms by which serine proteases alter lung fluid clearance in rat lungs and vectorial ion transport in airway and alveolar epithelial cells. Inhibition of endogenous protease activity by intratracheal instillation of soybean trypsin inhibitor (SBTI) or α1-antitrypsin decreased amiloride-sensitive lung fluid clearance across rat fluid-filled lungs; instillation of trypsin partially restored this effect. Gelatin zymography demonstrated SBTI-inhibitable trypsin-like activity in rat lung lavage fluid. Apical trypsin and human neutrophil elastase, but not agonists of protea

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Fukui, Eriko, Soichiro Funaki, Kenji Kimura, et al. "Adipose Tissue-Derived Stem Cells Have the Ability to Differentiate into Alveolar Epithelial Cells and Ameliorate Lung Injury Caused by Elastase-Induced Emphysema in Mice." Stem Cells International 2019 (June 10, 2019): 1–14. http://dx.doi.org/10.1155/2019/5179172.

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Chronic obstructive pulmonary disease is a leading cause of mortality globally, with no effective therapy yet established. Adipose tissue-derived stem cells (ADSCs) are useful for ameliorating lung injury in animal models. However, whether ADSCs differentiate into functional cells remains uncertain, and no study has reported on the mechanism by which ADSCs improve lung functionality. Thus, in this study, we examined whether ADSCs differentiate into lung alveolar cells and are able to ameliorate lung injury caused by elastase-induced emphysema in model mice. Here, we induced ADSCs to differenti

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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 (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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Glassberg, Marilyn K., Rhea Choi, Vita Manzoli та ін. "17β-Estradiol Replacement Reverses Age-Related Lung Disease in Estrogen-Deficient C57BL/6J Mice". Endocrinology 155, № 2 (2014): 441–48. http://dx.doi.org/10.1210/en.2013-1345.

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The role that estrogens play in the aging lung is poorly understood. Remodeling of the aging lung with thickening of the alveolar walls and reduction in the number of peripheral airways is well recognized. The present study was designed to address whether estrogen deficiency would affect age-associated changes in the lungs of female C57BL/6J mice. Lungs isolated from old mice (24 months old, estrogen-deficient) demonstrated decreased lung volume and decreased alveolar surface area. There was no difference in alveolar number in the lungs of old and young mice (6 months old, estrogen-replete). E

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Vrolyk, V., B. K. Wobeser, A. N. Al-Dissi, A. Carr, and B. Singh. "Lung Inflammation Associated With Clinical Acute Necrotizing Pancreatitis in Dogs." Veterinary Pathology 54, no. 1 (2016): 129–40. http://dx.doi.org/10.1177/0300985816646432.

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Although dogs with acute necrotizing pancreatitis (ANP) can develop respiratory complications, there are no data describing lung injury in clinical cases of ANP in dogs. Therefore, we conducted a study to characterize lung injury and determine if pulmonary intravascular macrophages (PIMs) are induced in dogs with ANP ( n = 21) compared with control dogs ( n = 6). Two pathologists independently graded histologic sections of pancreas from clinical cases to characterize the severity of ANP (total scores of 3–10) compared with controls showing histologically normal pancreas (total scores of 0). Ba

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Kim, Seong Chul, Thomas Kellett, Shaohua Wang, et al. "TRIM72 is required for effective repair of alveolar epithelial cell wounding." American Journal of Physiology-Lung Cellular and Molecular Physiology 307, no. 6 (2014): L449—L459. http://dx.doi.org/10.1152/ajplung.00172.2014.

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The molecular mechanisms for lung cell repair are largely unknown. Previous studies identified tripartite motif protein 72 (TRIM72) from striated muscle and linked its function to tissue repair. In this study, we characterized TRIM72 expression in lung tissues and investigated the role of TRIM72 in repair of alveolar epithelial cells. In vivo injury of lung cells was introduced by high tidal volume ventilation, and repair-defective cells were labeled with postinjury administration of propidium iodide. Primary alveolar epithelial cells were isolated and membrane wounding and repair were labeled

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Quan, Rui, Chenhong Shi, Bing Fang, et al. "Age-Dependent Inflammatory Microenvironment Mediates Alveolar Regeneration." International Journal of Molecular Sciences 25, no. 6 (2024): 3476. http://dx.doi.org/10.3390/ijms25063476.

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Lung aging triggers the onset of various chronic lung diseases, with alveolar repair being a key focus for alleviating pulmonary conditions. The regeneration of epithelial structures, particularly the differentiation from type II alveolar epithelial (AT2) cells to type I alveolar epithelial (AT1) cells, serves as a prominent indicator of alveolar repair. Nonetheless, the precise role of aging in impeding alveolar regeneration and its underlying mechanism remain to be fully elucidated. Our study employed histological methods to examine lung aging effects on structural integrity and pathology. L

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Wang, Limei, Patrick Dorn, Cedric Simillion, et al. "EpCAM+CD73+ mark epithelial progenitor cells in postnatal human lung and are associated with pathogenesis of pulmonary disease including lung adenocarcinoma." American Journal of Physiology-Lung Cellular and Molecular Physiology 319, no. 5 (2020): L794—L809. http://dx.doi.org/10.1152/ajplung.00279.2019.

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Lung injury in mice induces mobilization of discrete subsets of epithelial progenitor cells to promote new airway and alveolar structures. However, whether similar cell types exist in human lung remains unresolved. Using flow cytometry, we identified a distinct cluster of cells expressing the epithelial cell adhesion molecule (EpCAM), a cell surface marker expressed on epithelial progenitor cells, enriched in the ecto-5′-nucleotidase CD73 in unaffected postnatal human lungs resected from pediatric patients with congenital lung lesions. Within the EpCAM+CD73+ population, a small subset coexpres

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Lopez, A., M. Prior, L. E. Lilue, C. Gulayets, and O. S. Atwal. "Histologic and Ultrastructural Alterations in Lungs of Rats Exposed to Sub-lethal Concentrations of Hydrogen Sulfide." Veterinary Pathology 25, no. 5 (1988): 376–84. http://dx.doi.org/10.1177/030098588802500507.

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Fischer-344 rats were killed 1, 18, and 42 hr after a single 4-hr exposure to an atmosphere of 0, 116, or 615 mg m-3 of hydrogen sulfide (H2S). Lungs, fixed by the intratracheal route, were examined by light and electron microscopy. Histologic changes were transient and mainly present in rats exposed to 615 mg m-3 H2S. Lesions included severe but transitory pulmonary edema and fibrinocellular alveolitis which was restricted to the proximal alveolar region of the lung. Electron microscopically, ciliated bronchiolar cells were the only cells that developed necrosis; they were rapidly replaced by

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Pavan, Eshwar Reddy K., Pragna K. Sravani, Kumar K. Pawan, et al. "Maladies of Respiration Effects and Progression of Emphysema, Life Expectancy of a Person with Emphysema, Stages, Symptoms, Diagnosis and Treatment of Emphysema." Journal of Surgical Nursing and Post Operative Nursing Care 1, no. 1 (2023): 40–44. https://doi.org/10.5281/zenodo.8001230.

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<em>Emphysema is related to the obstructive type of respiratory disease. In the condition, the destruction of lung tissues happens and directs towards the loss of alveolar walls. Due to the above property, the loss of the elastic recoil of lungs also takes place. Emphysema is observed due to the smoke or oxidant gases, an enhancement of the mucus secretion from the epithelial cells, partial paralysis of the cells of the respiratory epithelial cells, the removal of alveolar mucus membrane and an elimination of elastic tissues. Bronchiolar damage leads to an enhancement of the airway resistance.

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Lkhagvadorj, Khosbayar, Zhijun Zeng, Juan Song, et al. "Prenatal smoke exposure dysregulates lung epithelial cell differentiation in mouse offspring: role for AREG-induced EGFR signaling." American Journal of Physiology-Lung Cellular and Molecular Physiology 319, no. 4 (2020): L742—L751. http://dx.doi.org/10.1152/ajplung.00209.2020.

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Prenatal smoke exposure is a risk factor for impaired lung development in children. Recent studies have indicated that amphiregulin (AREG), which is a ligand of the epidermal growth factor receptor (EGFR), has a regulatory role in airway epithelial cell differentiation. In this study, we investigated the effect of prenatal smoke exposure on lung epithelial cell differentiation and linked this with AREG-EGFR signaling in 1-day-old mouse offspring. Bronchial and alveolar epithelial cell differentiations were assessed by immunohistochemistry. Areg, epidermal growth factor ( Egf), and mRNA express

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Hardie, William D., Pablo A. Bejarano, Mary Ann Miller, et al. "Immunolocalization of Transforming Growth Factor a and Epidermal Growth Factor Receptor in Lungs of Patients with Cystic Fibrosis." Pediatric and Developmental Pathology 2, no. 5 (1999): 415–23. http://dx.doi.org/10.1007/s100249900144.

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Transforming growth factor α (TGF-α) is expressed in respiratory epithelial cells and alveolar macrophages during development and following lung injury. In the present study the presence and sites of synthesis of TGF-α and its receptor, the epidermal growth factor receptor (EGF-R), were assessed in lung tissue from patients with severe lung disease caused by cystic fibrosis (CF). Lung sections from 24 individuals with CF, obtained at the time of lung transplantation, were compared to lung sections from five lung donors without CF. Cellular sites of TGF-α, EGF-R, and cellular sites of prolifera

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Bates, S. R., and A. B. Fisher. "Surfactant protein A is degraded by alveolar macrophages." American Journal of Physiology-Lung Cellular and Molecular Physiology 271, no. 2 (1996): L258—L266. http://dx.doi.org/10.1152/ajplung.1996.271.2.l258.

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The metabolism of iodinated lung surfactant protein A (SP-A) by alveolar macrophages in primary culture was examined to determine the role these cells play in the degradation of this surfactant protein. SP-A was isolated from lung lavage obtained from normal bovines, patients with alveolar proteinosis, and silica-treated rats. SP-A (0.5 microgram/ml) was incubated for 3 h with rat alveolar macrophages obtained by lung lavage. Cell association and degradation of human and rat SP-A was three times greater than that of bovine SP-A. During the 3-h period, 50% of total macrophage-associated SP-A wa

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Lubman, R. L., and E. D. Crandall. "Regulation of intracellular pH in alveolar epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 262, no. 1 (1992): L1—L14. http://dx.doi.org/10.1152/ajplung.1992.262.1.l1.

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Alveolar type II epithelial cells in adult mammalian lungs actively transport salt and water, secrete surfactant, and differentiate into type I cells under normal conditions and following lung injury. It has become increasingly apparent that, like all epithelial cells, alveolar pneumocytes have evolved specialized ion transport mechanisms by which they regulate their intracellular pH (pHi). pHi is an important biological parameter in all living cells whose regulation is necessary for normal cellular homeostasis. pHi, and the ion transport mechanisms by which it is regulated, may contribute to

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Bolasco, Giulia, Dhani C. Tracey-White, Tanya Tolmachova, et al. "Loss of Rab27 function results in abnormal lung epithelium structure in mice." American Journal of Physiology-Cell Physiology 300, no. 3 (2011): C466—C476. http://dx.doi.org/10.1152/ajpcell.00446.2010.

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Rab27 small GTPases regulate secretion and movement of lysosome-related organelles such as T cell cytolytic granules and platelet-dense granules. Previous studies indicated that Rab27a and Rab27b are expressed in the murine lung suggesting that they regulate secretory processes in the lung. Consistent with those studies, we found that Rab27a and Rab27b are expressed in cell types that contain secretory granules: alveolar epithelial type II (AEII) and Clara cells. We then used Rab27a/Rab27b double knockout (DKO) mice to examine the functional consequence of loss of Rab27 proteins in the murine

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Ribeiro Baptista, B., J. Grégoire, M. Toigo, et al. "Lung alveolar regeneration by p16 deletion in alveolar epithelial cells." Revue des Maladies Respiratoires 40, no. 2 (2023): 114. http://dx.doi.org/10.1016/j.rmr.2022.11.012.

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Hollenhorst, Monika I., Katrin Richter, and Martin Fronius. "Ion Transport by Pulmonary Epithelia." Journal of Biomedicine and Biotechnology 2011 (2011): 1–16. http://dx.doi.org/10.1155/2011/174306.

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The lung surface of air-breathing vertebrates is formed by a continuous epithelium that is covered by a fluid layer. In the airways, this epithelium is largely pseudostratified consisting of diverse cell types such as ciliated cells, goblet cells, and undifferentiated basal cells, whereas the alveolar epithelium consists of alveolar type I and alveolar type II cells. Regulation and maintenance of the volume and viscosity of the fluid layer covering the epithelium is one of the most important functions of the epithelial barrier that forms the outer surface area of the lungs. Therefore, the epit

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Andrade, Cristiano F., Amy P. Wong, Thomas K. Waddell, Shaf Keshavjee, and Mingyao Liu. "Cell-based tissue engineering for lung regeneration." American Journal of Physiology-Lung Cellular and Molecular Physiology 292, no. 2 (2007): L510—L518. http://dx.doi.org/10.1152/ajplung.00175.2006.

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Emphysema is a chronic lung disease characterized by alveolar enlargement and tissue loss. Tissue engineering represents an attractive potential for regeneration of several organ systems. The complex three-dimensional architectural structure of lung parenchyma requiring connections of alveolar units to airways and the pulmonary circulation makes this strategy less optimistic. In the present study, we used Gelfoam sponge as a scaffold material, supplemented with fetal rat lung cells as progenitors, to explore the potential application of cell-based tissue engineering for lung regeneration in ad

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Jobe, Alan H. "The Alveolar Lining Layer: A Review of Studies on Its Role in Pulmonary Mechanics and in the Pathogenesis of Atelectasis, by Mary Ellen Avery, MD, Pediatrics, 1962:30:324–330." Pediatrics 102, Supplement_1 (1998): 234–36. http://dx.doi.org/10.1542/peds.102.s1.234.

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The alveoli of the normal lung are lined by a substance that exerts surface tension at the air–liquid interface. In the expanded lung, the tension is high and operates to increase the elastic recoil of the lung. In the lung at low volumes, the surface tension becomes extremely low. This confers stability on the air spaces and thus prevents atelectasis. This lining layer is a lipoprotein film, which is not found where alveoli still are lined by cuboidal epithelium. Its appearance coincides with the appearance of alveolar lining cells. Electron microscopic evidence of secretory activity in alveo

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