Detection of Antibodies in Serum of Patients with Idiopathic Pulmonary Fibrosis against Isolated Rat Alveolar Type II Cells

Respiration ◽  
1987 ◽  
Vol 52 (2) ◽  
pp. 122-128 ◽  
Author(s):  
U. Baumgartner ◽  
J. Schölmerich ◽  
S. Becker ◽  
U. Costabel
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Isolated Rat

scholarly journals Alveolar epithelial cells express mesenchymal proteins in patients with idiopathic pulmonary fibrosis

2011 ◽  
Vol 301 (1) ◽  
pp. L71-L78 ◽  
Author(s):  
Cecilia Marmai ◽  
Rachel E. Sutherland ◽  
Kevin K. Kim ◽  
Gregory M. Dolganov ◽  
Xiaohui Fang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Mesenchymal Cells ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Mesenchymal Transition

Prior work has shown that transforming growth factor-β (TGF-β) can mediate transition of alveolar type II cells into mesenchymal cells in mice. Evidence this occurs in humans is limited to immunohistochemical studies colocalizing epithelial and mesenchymal proteins in sections of fibrotic lungs. To acquire further evidence that epithelial-to-mesenchymal transition occurs in the lungs of patients with idiopathic pulmonary fibrosis (IPF), we studied alveolar type II cells isolated from fibrotic and normal human lung. Unlike normal type II cells, type II cells isolated from the lungs of patients with IPF express higher levels of mRNA for the mesenchymal proteins type I collagen, α-smooth muscle actin (α-SMA), and calponin. When cultured on Matrigel/collagen, human alveolar type II cells maintain a cellular morphology consistent with epithelial cells and expression of surfactant protein C (SPC) and E-cadherin. In contrast, when cultured on fibronectin, the human type II cells flatten, spread, lose expression of pro- SPC, and increase expression of vimentin, N-cadherin, and α-SMA; markers of mesenchymal cells. Addition of a TGF-β receptor kinase inhibitor (SB431542) to cells cultured on fibronectin inhibited vimentin expression and maintained pro-SPC expression, indicating persistence of an epithelial phenotype. These data suggest that alveolar type II cells can acquire features of mesenchymal cells in IPF lungs and that TGF-β can mediate this process.

scholarly journals Phospholipid-transfer activities in cytosols from lung, isolated alveolar type II cells and alveolar type II cell-derived adenomas

1983 ◽  
Vol 215 (3) ◽  
pp. 637-642 ◽  
Author(s):  
G L Pool ◽  
D G Bubacz ◽  
R H Lumb ◽  
R J Mason
Keyword(s):  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Transfer Protein ◽  
Alveolar Type Ii Cell ◽  
Phospholipid Transfer ◽  
Type Ii Cell ◽  
Specific Proteins ◽  
Isolated Rat

We have examined phospholipid-transfer activities in cytosols from rat and mouse whole lung, isolated rat alveolar type II cells and alveolar type II cell-derived mouse pulmonary adenomas. We report an enrichment in phosphatidylcholine and phosphatidylglycerol (but not phosphatidylinositol) protein-catalysed transfer in the type II cell and adenoma cytosols compared with the whole-lung cytosols. The activities from these cytosols were resolved using column chromatofocusing, which clearly demonstrated the presence of a phosphatidylcholine-specific transfer protein in each of the four tissues. In addition, two proteins (rat) or three proteins (mouse) catalysing both phosphatidylcholine and phosphatidylglycerol transfer were resolved from whole lung, whereas in both the rat isolated alveolar type II cells and the mouse type II cell-derived adenomas one of these less specific proteins is not present.

scholarly journals Meconium Increases Surfactant Secretion in Isolated Rat Alveolar Type II Cells

1996 ◽  
Vol 39 (3) ◽  
pp. 443-447 ◽  
Author(s):  
Stephen T Higgins ◽  
Ai-Min Wu ◽  
Namita Sen ◽  
Alan R Spitzer ◽  
Avinash Chander
Keyword(s):  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Surfactant Secretion ◽  
Isolated Rat

scholarly journals Therapeutic effects of telomerase in mice with pulmonary fibrosis induced by damage to the lungs and short telomeres

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Juan Manuel Povedano ◽  
Paula Martinez ◽  
Rosa Serrano ◽  
Águeda Tejera ◽  
Gonzalo Gómez-López ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Tissue Regeneration ◽  
Low Dose ◽  
Alveolar Type ◽  
Therapeutic Effects ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Sporadic Cases ◽  
Inflammatory Infiltrates

Pulmonary fibrosis is a fatal lung disease characterized by fibrotic foci and inflammatory infiltrates. Short telomeres can impair tissue regeneration and are found both in hereditary and sporadic cases. We show here that telomerase expression using AAV9 vectors shows therapeutic effects in a mouse model of pulmonary fibrosis owing to a low-dose bleomycin insult and short telomeres. AAV9 preferentially targets regenerative alveolar type II cells (ATII). AAV9-Tert-treated mice show improved lung function and lower inflammation and fibrosis at 1–3 weeks after viral treatment, and improvement or disappearance of the fibrosis at 8 weeks after treatment. AAV9-Tert treatment leads to longer telomeres and increased proliferation of ATII cells, as well as lower DNA damage, apoptosis, and senescence. Transcriptome analysis of ATII cells confirms downregulation of fibrosis and inflammation pathways. We provide a proof-of-principle that telomerase activation may represent an effective treatment for pulmonary fibrosis provoked or associated with short telomeres.

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