Hypertrophy and Hyperplasia of Alveolar Type II Cells in Response to Silica and Other Pulmonary Toxicants

Miller, Bruce E.; Hook, Gary E. R.

doi:10.2307/3430661

Cited by 50 publications

(39 citation statements)

References 34 publications

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“…This histopathological finding is compatible with the significantly increased ALP activity in the BAL fluid throughout the 91-d post-exposure period, since enhanced ALP activity has been reported to reflect secretory activity of Type II pneumocytes 15,33) . The present result is also consistent with the findings of Shvedova et al that pharyngeal aspiration of SWCNT in mice increased the immunofluorescentce of cytokeratins 8/18 and markers of Type II epithelial cells in the alveolus, and the number of cells expressing cytoplasmic lamellar bodies in TEM sections.…”

Section: Discussionsupporting

confidence: 86%

Pulmonary Toxicity of Intratracheally Instilled Multiwall Carbon Nanotubes in Male Fischer 344 Rats

et al. 2010

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Section: Discussionsupporting

confidence: 86%

Pulmonary Toxicity of Intratracheally Instilled Multiwall Carbon Nanotubes in Male Fischer 344 Rats

et al. 2010

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“…The proliferation of type II cells in A Ϫ D Ϫ mice might be a reaction to lung inflammation. In different models of acute and chronic lung inflammation, type II cell proliferation and hypertrophy were demonstrated (Miller and Hook, 1990;Bryson et al, 1991;Kasper and Haroske, 1996;Fehrenbach, 2001;Homer et al, 2002). In human lung emphysema, the rate of proliferation of alveolar epithelial cells is enhanced (Yokohori et al., 2004).…”

Section: Discussionmentioning

confidence: 99%

Design‐based stereological analysis of the lung parenchymal architecture and alveolar type II cells in surfactant protein A and D double deficient mice

et al. 2005

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Alveolar epithelial type II cells synthesize and secrete surfactant. The surfactant-associated proteins A and D (SP-A and SP-D), members of the collectin protein family, participate in pulmonary immune defense, modulation of inflammation, and surfactant metabolism. Both proteins are known to have overlapping as well as distinct functions. The present study provides a design-based stereological analysis of adult mice deficient in both SP-A and SP-D (A Ϫ D Ϫ ) with special emphasis on parameters characterizing alveolar architecture and surfactant-producing type II cells. Compared to wild-type, A Ϫ D Ϫ mice have fewer and larger alveoli, an increase in the number and size of type II cells, as well as more numerous and larger alveolar macrophages. More surfactant-storing lamellar bodies are seen in type II cells, leading to a threefold increase in the total volume of lamellar bodies per lung, but the mean volume of a single lamellar body remains constant. These results demonstrate that chronic deficiency of SP-A and SP-D in mice leads to parenchymal remodeling, type II cell hyperplasia and hypertrophy, and disturbed intracellular surfactant metabolism. The design-based stereological approach presented here provides a framework for the quantitative lung structure analysis in gene-manipulated mice as well as in human lung disease.

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“…The protocol for pulmonary epithelial cells isolation from neonatal rats was the same as that for fetal lungs, except that 0.036 units/ml elastase was included in the digestion enzyme solution. The purity of the isolated fetal pulmonary epithelial cells cells was 90 ~ 95% as determined by alkaline phosphatase staining (Miller and Hook, 1990) and FITC-labeled Maclura pomifera agglutinin staining. The viability was >90% as determined by Trypan blue exclusion.…”

Section: Collection Of Fetal Lung Tissues and Isolation Of Fetal Pulmmentioning

confidence: 99%

Ionotropic GABA receptor expression in the lung during development

Jin

Guo

Sun

et al. 2008

Gene Expression Patterns

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Cl − transport is essential for lung development. Because gamma-aminobutyric acid (GABA) receptors allow the flow of negatively-charged Cl − ions across the cell membrane, we hypothesized that the expression of ionotropic GABA receptors are regulated in the lungs during development. We identified 17 GABA receptor subunits in the lungs by real-time PCR. These subunits were categorized into 4 groups: Group 1 had high mRNA expression during fetal stages and low in adults; Group 2 had steady expression to adult stages with a slight up-regulation at birth; Group 3 showed an increasing expression from fetal to adult lungs; and Group 4 displayed irregular mRNA fluctuations. The protein levels of selected subunits were also determined by Western blots and some subunits had protein levels that corresponded to mRNA levels. Further studied subunits were primarily localized in epithelial cells in the developing lung with differential mRNA expression between isolated cells and whole lung tissues. Our results add to the knowledge of GABA receptor expression in the lung during development. Keywordslungs; ionotropic GABA receptor; fetal lung development; chloride homeostasis; lung fluid transport; real time PCR; gene expression; alveolar epithelial cells RESULTS AND DISCUSSION SignificanceCl − channels play an important role in the lung throughout an animal's life. During the fetal stages, the lung is a fluid-secreting organ. The main driving force for fluid secretion is the active secretion of Cl − into the developing lungs. Therefore, Cl − channels are indispensable for fetal lung development and morphogenesis (Folkesson et al., 1998;Olver et al., 2004;Bland and Nielson, 1992). On the other hand, the adult lung is air-filled and maintains a "dry" state. The apical surface is covered by a thin layer of alveolar surface fluid. This layer of fluid is required for the proper air exchange and airway defenses. Cl − channels are also essential for maintaining the composition and volume of the alveolar surface fluid (Brochiero et al., 2004 Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Several Cl − channels have previously been studied in the lung. The cystic fibrosis transmembrane conductance regulator (CFTR) (Harris et al., 1991), the voltage-gated Cl − channels, ClC2 (Thiemann et al., 1992), ClC3 (Lamb et al., 2001), and ClC5 (Edmonds et al., 2002, and Na + -K + -Cl − cotransporter (NKCC) (Rochelle et al., 2000) have been detected in fetal lungs, distal airway epithelial cells and alveolar epithelial cells. Some of the channels have been shown to be involved in fluid homeostasis i...

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Hypertrophy and Hyperplasia of Alveolar Type II Cells in Response to Silica and Other Pulmonary Toxicants

Cited by 50 publications

References 34 publications

Pulmonary Toxicity of Intratracheally Instilled Multiwall Carbon Nanotubes in Male Fischer 344 Rats

Pulmonary Toxicity of Intratracheally Instilled Multiwall Carbon Nanotubes in Male Fischer 344 Rats

Design‐based stereological analysis of the lung parenchymal architecture and alveolar type II cells in surfactant protein A and D double deficient mice

Ionotropic GABA receptor expression in the lung during development

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