Differentiating Type i and Type ii Alveolar Cells in Rat Lung by OsO4NaI Staining

1970 ◽  
Vol 45 (5) ◽  
pp. 215-219 ◽  
Author(s):  
William F. McNary ◽  
Al-Walid El-Bermani
Keyword(s):  
Type I ◽  
Type Ii ◽  
Rat Lung ◽  
Alveolar Cells ◽  
Type Ii Alveolar Cells

Integrin mediation of type II cell adherence to provisional matrix proteins

1996 ◽  
Vol 271 (2) ◽  
pp. L277-L286 ◽  
Author(s):  
H. J. Kim ◽  
D. H. Ingbar ◽  
C. A. Henke
Keyword(s):  
Cell Adhesion ◽  
Matrix Proteins ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Cells ◽  
Type Ii Cell ◽  
Type Ii Alveolar Cells ◽  
Alpha V Beta 3

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.

scholarly journals Type I collagen formation in rat type II alveolar cells immortalised by viral gene products.

Thorax ◽  
1994 ◽  
Vol 49 (3) ◽  
pp. 201-206 ◽  
Author(s):  
R Matsui ◽  
R H Goldstein ◽  
K Mihal ◽  
J S Brody ◽  
M P Steele ◽  
...  
Keyword(s):  
Type I Collagen ◽  
Viral Gene ◽  
Type I ◽  
Gene Products ◽  
Type Ii ◽  
Alveolar Cells ◽  
Collagen Formation ◽  
Type Ii Alveolar Cells

scholarly journals Respiratory Failure Due to Differentiation Arrest and Expansion of Alveolar Cells following Lung-Specific Loss of the Transcription Factor C/EBPα in Mice

2006 ◽  
Vol 26 (3) ◽  
pp. 1109-1123 ◽  
Author(s):  
Daniela S. Bassères ◽  
Elena Levantini ◽  
Hongbin Ji ◽  
Stefano Monti ◽  
Shannon Elf ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Differentiation ◽  
Respiratory Failure ◽  
Leucine Zipper ◽  
Type I ◽  
Type Ii ◽  
Alveolar Cells ◽  
Proliferating Cells ◽  
Therapeutic Benefits ◽  
Factor C

ABSTRACT The leucine zipper family transcription factor CCAAT enhancer binding protein alpha (C/EBPα) inhibits proliferation and promotes differentiation in various cell types. In this study, we show, using a lung-specific conditional mouse model of C/EBPα deletion, that loss of C/EBPα in the respiratory epithelium leads to respiratory failure at birth due to an arrest in the type II alveolar cell differentiation program. This differentiation arrest results in the lack of type I alveolar cells and differentiated surfactant-secreting type II alveolar cells. In addition to showing a block in type II cell differentiation, the neonatal lungs display increased numbers of proliferating cells and decreased numbers of apoptotic cells, leading to epithelial expansion and loss of airspace. Consistent with the phenotype observed, genes associated with alveolar maturation, survival, and proliferation were differentially expressed. Taken together, these results identify C/EBPα as a master regulator of airway epithelial maturation and suggest that the loss of C/EBPα could also be an important event in the multistep process of lung tumorigenesis. Furthermore, this study indicates that exploring the C/EBPα pathway might have therapeutic benefits for patients with respiratory distress syndromes.

scholarly journals Bradykinin Stimulates Type II Alveolar Cells to Release Neutrophil and Monocyte Chemotactic Activity and Inflammatory Cytokines

1998 ◽  
Vol 153 (6) ◽  
pp. 1885-1893 ◽  
Author(s):  
Sekiya Koyama ◽  
Etsuro Sato ◽  
Hiroshi Nomura ◽  
Keishi Kubo ◽  
Masakazu Miura ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Chemotactic Activity ◽  
Type Ii ◽  
Alveolar Cells ◽  
Type Ii Alveolar Cells

PM2.5-induced lung inflammation in mice: Differences of inflammatory response in macrophages and type II alveolar cells

2017 ◽  
Vol 37 (10) ◽  
pp. 1203-1218 ◽  
Author(s):  
Miao He ◽  
Takamichi Ichinose ◽  
Seiichi Yoshida ◽  
Tomohiro Ito ◽  
Cuiying He ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Lung Inflammation ◽  
Type Ii ◽  
Alveolar Cells ◽  
Type Ii Alveolar Cells

scholarly journals CD8+ T Cell–mediated Injury In Vivo Progresses in the Absence of Effector T Cells

2001 ◽  
Vol 194 (12) ◽  
pp. 1835-1846 ◽  
Author(s):  
Barbara A. Small ◽  
Sarah A. Dressel ◽  
Christopher W. Lawrence ◽  
Donald R. Drake ◽  
Mark H. Stoler ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Tissue Injury ◽  
Cd8 T Cell ◽  
Effector T Cells ◽  
Type Ii ◽  
Pulmonary Injury ◽  
Alveolar Cells ◽  
Type Ii Alveolar Cells

Tissue injury is a common sequela of acute virus infection localized to a specific organ such as the lung. Tissue injury is an immediate consequence of infection with lytic viruses. It can also result from the direct destruction of infected cells by effector CD8+ T lymphocytes and indirectly through the action of the T cell–derived proinflammatory cytokines and recruited inflammatory cells on infected and uninfected tissue. We have examined CD8+ T cell–mediated pulmonary injury in a transgenic model in which adoptively transferred, virus-specific cytotoxic T lymphocytes (CTLs) produce lethal, progressive pulmonary injury in recipient mice expressing the viral target transgene exclusively in the lungs. We have found that over the 4–5 day course of the development of lethal pulmonary injury, the effector CTLs, while necessary for the induction of injury, are present only transiently (24–48 h) in the lung. We provide evidence that the target of the antiviral CD8+ T cells, the transgene expressing type II alveolar cells, are not immediately destroyed by the effector T cells. Rather, after T cell–target interaction, the type II alveolar cells are stimulated to produce the chemokine monocyte chemoattractant protein 1. These results reinforce the concept that, in vivo, the cellular targets of specific CTLs may participate directly in the development of progressive tissue injury by activating in response to interaction with the T cells and producing proinflammatory mediators without sustained in vivo activation of CD8+ T cell effectors.

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