Regulation of intracellular pH in alveolar epithelial cells

1992 ◽  
Vol 262 (1) ◽  
pp. L1-L14 ◽  
Author(s):  
R. L. Lubman ◽  
E. D. Crandall
Keyword(s):  
Epithelial Cells ◽  
Ion Transport ◽  
Cell Volume ◽  
Intracellular Ph ◽  
Type I ◽  
Transport Mechanisms ◽  
Alveolar Epithelial ◽  
Cellular Processes ◽  
Proliferation And Differentiation ◽  
Phi Regulation

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 many cellular processes, including transcellular transport, cell volume and osmolarity regulation, and intracellular transport, cell volume and osmolarity regulation, and intracellular electrolyte composition. Moreover, changes in pHi may serve as intracellular signals for biological processes such as cell growth, proliferation, and differentiation. We review herein the general principles of pHi regulation in epithelia and describe the mechanisms and effects of pHi regulation in alveolar pneumocytes. Many of the critical issues in current pulmonary research involve processes that pHi is most likely to affect, including maintenance of alveolar epithelial barrier integrity, development and maintenance of epithelial polarity, epithelial proliferation and differentiation, and regulation of transepithelial transport with respect to alveolar fluid balance in normal individuals and in those with excess alveolar fluid (i.e., pulmonary edema). Investigations into the regulation of pHi in alveolar pneumocytes and the regulatory effects of pHi in turn on other cellular processes are likely to yield information important to the understanding of lung biology and pulmonary disease.

Disparate cytokine regulation of ICAM-1 in rat alveolar epithelial cells and pulmonary endothelial cells in vitro

1995 ◽  
Vol 269 (1) ◽  
pp. L127-L135 ◽  
Author(s):  
W. W. Barton ◽  
S. Wilcoxen ◽  
P. J. Christensen ◽  
R. Paine
Keyword(s):  
Endothelial Cells ◽  
Epithelial Cells ◽  
Inflammatory Cytokines ◽  
Alveolar Epithelial Cells ◽  
Normal Lung ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Epithelial

Intercellular adhesion molecule-1 (ICAM-1) is expressed at high levels on type I alveolar epithelial cells in the normal lung and is induced in vitro as type II cells spread in primary culture. In contrast, in most nonhematopoetic cells ICAM-1 expression is induced in response to inflammatory cytokines. We have formed the hypothesis that the signals that control ICAM-1 expression in alveolar epithelial cells are fundamentally different from those controlling expression in most other cells. To test this hypothesis, we have investigated the influence of inflammatory cytokines on ICAM-1 expression in isolated type II cells that have spread in culture and compared this response to that of rat pulmonary artery endothelial cells (RPAEC). ICAM-1 protein, determined both by a cell-based enzyme-linked immunosorbent assay and by Western blot analysis, and mRNA were minimally expressed in unstimulated RPAEC but were significantly induced in a time- and dose-dependent manner by treatment with tumor necrosis factor-alpha, interleukin-1 beta, or interferon-gamma. In contrast, these cytokines did not influence the constitutive high level ICAM-1 protein expression in alveolar epithelial cells and only minimally affected steady-state mRNA levels. ICAM-1 mRNA half-life, measured in the presence of actinomycin D, was relatively long at 7 h in alveolar epithelial cells and 4 h in RPAEC. The striking lack of response of ICAM-1 expression by alveolar epithelial cells to inflammatory cytokines is in contrast to virtually all other epithelial cells studied to date and supports the hypothesis that ICAM-1 expression by these cells is a function of cellular differentiation.(ABSTRACT TRUNCATED AT 250 WORDS)

Pneumonia in Lambs Inoculated with Bordetella parapertussis: Bronchoalveolar Lavage and Ultrastructural Studies

1988 ◽  
Vol 25 (4) ◽  
pp. 297-303 ◽  
Author(s):  
W. Chen ◽  
M. R. Alley ◽  
B. W. Manktelow ◽  
D. Hopcroft ◽  
R. Bennett
Keyword(s):  
Epithelial Cells ◽  
Bronchoalveolar Lavage ◽  
Alveolar Macrophages ◽  
Bronchial Epithelium ◽  
Alveolar Epithelial Cells ◽  
Type I ◽  
Bordetella Parapertussis ◽  
Alveolar Epithelial ◽  
Ultrastructural Studies ◽  
Cell Counts

Eight colostrum-deprived lambs were inoculated intratracheally with ovine isolates of Bordetella parapertussis. Fluids obtained by bronchoalveolar lavage had a large increase in total cell counts 24 hours after inoculation; up to 93% of cells were neutrophils. From 3 days after inoculation, the number of alveolar macrophages in lavage samples was markedly increased. From 5 days onwards, many alveolar macrophages had moderate to severe cytoplasmic vacuolation. Topographically, tracheal and bronchial epithelium was covered by a large amount of inflammatory exudate 24 hours after inoculation. Later, the tracheobronchial epithelium showed focal extrusions from ciliated cells, which were occasionally associated with B. parapertussis organisms. Ultrastructurally, cytopathological changes associated with B. parapertussis infection were mild focal degeneration of airway epithelium with slight loss of cilia, moderate to severe degeneration of type I and type II alveolar epithelial cells, and focal inflammation in the lungs. These results suggest that the primary targets of B. parapertussis infection are alveolar macrophages and the epithelial cells of bronchioles and alveoli.

scholarly journals Hypoxia regulates gene expression of alveolar epithelial transport proteins

2000 ◽  
Vol 88 (5) ◽  
pp. 1890-1896 ◽  
Author(s):  
Christine Clerici ◽  
Michael A. Matthay
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Alveolar Epithelium ◽  
Transport Proteins ◽  
Alveolar Epithelial Cells ◽  
Type I ◽  
Type Ii ◽  
Atp Content ◽  
Glut 1 ◽  
Alveolar Epithelial

Alveolar hypoxia occurs during ascent to high altitude but is also commonly observed in many acute and chronic pulmonary disorders. The alveolar epithelium is directly exposed to decreases in O2tension, but a few studies have evaluated the effects of hypoxia on alveolar cell function. The alveolar epithelium consists of two cell types: large, flat, squamous alveolar type I and cuboidal type II (ATII). ATII cells are more numerous and have a number of critical functions, including transporting ions and substrates required for many physiological processes. ATII cells express 1) membrane proteins used for supplying substrates required for cell metabolism and 2) ion transport proteins such as Na+channels and Na+-K+-ATPase, which are involved in the vectorial transport of Na+from the alveolar to interstitial spaces and therefore drive the resorption of alveolar fluid. This brief review focuses on gene expression regulation of glucose transporters and Na+transport proteins by hypoxia in alveolar epithelial cells. Cells exposed to severe hypoxia (0% or 3% O2) for 24 h upregulate the activity and expression of the glucose transporter GLUT-1, resulting in preservation of ATP content. Hypoxia-induced increases in GLUT-1 mRNA levels are due to O2deprivation and inhibition of oxidative phosphorylation. This regulation occurs at the transcriptional level through activation of a hypoxia-inducible factor. In contrast, hypoxia downregulates expression and activity of Na+channels and Na+-K+-ATPase in cultured alveolar epithelial cells. Hypoxia induces time- and concentration-dependent decreases of α-, β-, and γ-subunits of epithelial Na+channel mRNA and β1- and α1-subunits of Na+-K+-ATPase, effects that are completely reversed after reoxygenation. The mechanisms by which O2deprivation regulates gene expression of Na+transport proteins are not fully elucidated but likely involve the redox status of the cell. Thus hypoxia regulates gene expression of transport proteins in cultured alveolar epithelial type II cells differently, preserving ATP content.

scholarly journals Radiation Induces Pulmonary Fibrosis by Promoting the Fibrogenic Differentiation of Alveolar Stem Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Lu-Kai Wang ◽  
Tsai-Jung Wu ◽  
Ji-Hong Hong ◽  
Fang-Hsin Chen ◽  
John Yu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Epithelial Cells ◽  
Epithelial Mesenchymal Transition ◽  
Tissue Growth ◽  
Alveolar Epithelial Cells ◽  
Type I ◽  
Alveolar Cells ◽  
Mesenchymal Transition ◽  
Alveolar Epithelial ◽  
Radiation Induced

The lung is a radiosensitive organ, which imposes limits on the therapeutic dose in thoracic radiotherapy. Irradiated alveolar epithelial cells promote radiation-related pneumonitis and fibrosis. However, the role of lung stem cells (LSCs) in the development of radiation-induced lung injury is still unclear. In this study, we found that both LSCs and LSC-derived type II alveolar epithelial cells (AECII) can repair radiation-induced DNA double-strand breaks, but the irradiated LSCs underwent growth arrest and cell differentiation faster than the irradiated AECII cells. Moreover, radiation drove LSCs to fibrosis as shown with the elevated levels of markers for epithelial-mesenchymal transition and myofibroblast (α-smooth muscle actin (α-SMA)) differentiation in in vitro and ex vivo studies. Increased gene expressions of connective tissue growth factor and α-SMA were found in both irradiated LSCs and alveolar cells, suggesting that radiation could induce the fibrogenic differentiation of LSCs. Irradiated LSCs showed an increase in the expression of surfactant protein C (SP-C), the AECII cell marker, and α-SMA, and irradiated AECII cells expressed SP-C and α-SMA. These results indicated that radiation induced LSCs to differentiate into myofibroblasts and AECII cells; then, AECII cells differentiated further into either myofibroblasts or type I alveolar epithelial cells (AECI). In conclusion, our results revealed that LSCs are sensitive to radiation-induced cell damage and may be involved in radiation-induced lung fibrosis.

scholarly journals Nanoparticle (NP) uptake by type I alveolar epithelial cells and their oxidant stress response

2009 ◽  
Vol 3 (4) ◽  
pp. 307-318 ◽  
Author(s):  
Beth A. VanWinkle ◽  
Karen L. De Mesy Bentley ◽  
Jonathan M. Malecki ◽  
Karlene K. Gunter ◽  
Irene M. Evans ◽  
...  
Keyword(s):  
Stress Response ◽  
Epithelial Cells ◽  
Oxidant Stress ◽  
Alveolar Epithelial Cells ◽  
Type I ◽  
Alveolar Epithelial

scholarly journals Lectin binding patterns to terminal sugars of rat lung alveolar epithelial cells.

1990 ◽  
Vol 38 (2) ◽  
pp. 233-244 ◽  
Author(s):  
D J Taatjes ◽  
L A Barcomb ◽  
K O Leslie ◽  
R B Low
Keyword(s):  
Epithelial Cells ◽  
Lectin Binding ◽  
Alveolar Epithelial Cells ◽  
Gold Complex ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Rat Lung ◽  
Alveolar Epithelial ◽  
I Cells

We used post-embedding cytochemical techniques to investigate the lectin binding profiles of rat lung alveolar epithelial cells. Sections from rat lung embedded in the hydrophilic resin Lowicryl K4M were incubated either directly with a lectin-gold complex or with an unlabeled lectin followed by a specific glycoprotein-gold complex. The binding patterns of the five lectins used could be divided into three categories according to their reactivity with alveolar epithelial cells: (a) the Limax flavus lectin and Ricinus communis I lectin bound to both type I and type II cell plasma membranes; (b) the Helix pomatia lectin and Sambucus nigra L. lectin bound to type II but not type I cells; and (c) the Erythrina cristagalli lectin reacted with type I cells but was unreactive with type II cells. The specificity of staining was assessed by control experiments, including pre-absorption of the lectins with various oligosaccharides and enzymatic pre-treatment of sections with highly purified glycosidases to remove specific sugar residues. The results demonstrate that these lectins can be used to distinguish between type I and type II cells and would therefore be useful probes for investigating cell dynamics during lung development and remodeling.

scholarly journals Modification of Type I Collagenous Gels by Alveolar Epithelial Cells

2000 ◽  
Vol 22 (6) ◽  
pp. 702-707 ◽  
Author(s):  
Takeshi Umino ◽  
Hangjun Wang ◽  
Yunkui Zhu ◽  
Xiangde Liu ◽  
Lidia S. Manouilova ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Alveolar Epithelial Cells ◽  
Type I ◽  
Alveolar Epithelial

scholarly journals The Important Role of Ion Transport System in Cervical Cancer

2021 ◽  
Vol 23 (1) ◽  
pp. 333
Author(s):  
Yih-Fung Chen ◽  
Meng-Ru Shen
Keyword(s):  
Cervical Cancer ◽  
Epithelial Cells ◽  
Ion Transport ◽  
Cell Volume ◽  
Volume Regulation ◽  
Gynecological Cancer ◽  
Cell Volume Regulation ◽  
Hpv Infection ◽  
Transport Processes ◽  
Transport Systems

Cervical cancer is a significant gynecological cancer and causes cancer-related deaths worldwide. Human papillomavirus (HPV) is implicated in the etiology of cervical malignancy. However, much evidence indicates that HPV infection is a necessary but not sufficient cause in cervical carcinogenesis. Therefore, the cellular pathophysiology of cervical cancer is worthy of study. This review summarizes the recent findings concerning the ion transport processes involved in cell volume regulation and intracellular Ca2+ homeostasis of epithelial cells and how these transport systems are themselves regulated by the tumor microenvironment. For cell volume regulation, we focused on the volume-sensitive Cl− channels and K+-Cl− cotransporter (KCC) family, important regulators for ionic and osmotic homeostasis of epithelial cells. Regarding intracellular Ca2+ homeostasis, the Ca2+ store sensor STIM molecules and plasma membrane Ca2+ channel Orai proteins, the predominant Ca2+ entry mechanism in epithelial cells, are discussed. Furthermore, we evaluate the potential of these membrane ion transport systems as diagnostic biomarkers and pharmacological interventions and highlight the challenges.

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