Influence of Phosphodiesterase-Inhibitor PDE4 Roflumilast N-Oxide on Surfactant Protein of human Alveolar Epithelial Cell Type II

Pneumologie ◽  
2012 ◽  
Vol 66 (11) ◽  
Author(s):  
K Hoehne ◽  
SJ Schließmann ◽  
A Kirschbaum ◽  
T Ploenes ◽  
J Müller-Quernheim ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Alveolar Epithelial Cell ◽  
Phosphodiesterase Inhibitor ◽  
Surfactant Protein ◽  
Type Ii ◽  
Cell Type ◽  
Epithelial Cell Type ◽  
Alveolar Epithelial ◽  
Human Alveolar Epithelial Cell

scholarly journals OC-STAMP Overexpression Drives Lung Alveolar Epithelial Cell Type II Senescence in Silicosis

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Tian Li ◽  
Xin-yu Yang ◽  
Ding-jie Xu ◽  
Zi-yi Gao ◽  
Yi-bing Gao ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Er Stress ◽  
Cellular Senescence ◽  
Alveolar Epithelial Cell ◽  
Type Ii ◽  
Cell Type ◽  
Mesenchymal Transition ◽  
Epithelial Cell Type ◽  
Alveolar Epithelial ◽  
Chronic Lung Diseases

Cellular senescence has been considered an important driver of many chronic lung diseases. However, the specific mechanism of cellular senescence in silicosis is still unknown. In the present study, silicotic rats and osteoclast stimulatory transmembrane protein (Ocstamp) overexpression of MLE-12 cells were used to explore the mechanism of OC-STAMP in cellular senescence in alveolar epithelial cell type II (AEC2). We found an increasing level of OC-STAMP in AEC2 of silicotic rats. Overexpression of Ocstamp in MLE-12 cells promoted epithelial-mesenchymal transition (EMT), endoplasmic reticulum (ER) stress, and cellular senescence. Myosin heavy chain 9 (MYH9) was a potential interacting protein of OC-STAMP. Knockdown of Ocstamp or Myh9 inhibited cellular senescence in MLE-12 cells transfected with pcmv6-Ocstamp. Treatment with 4-phenylbutyrate (4-PBA) to inhibit ER stress also attenuated cellular senescence in vitro or in vivo. In conclusion, OC-STAMP promotes cellular senescence in AEC2 in silicosis.

Changes in alveolar epithelial cell proportions during fetal and postnatal development in sheep

2003 ◽  
Vol 285 (3) ◽  
pp. L664-L670 ◽  
Author(s):  
S. J. Flecknoe ◽  
M. J. Wallace ◽  
M. L. Cock ◽  
R. Harding ◽  
S. B. Hooper
Keyword(s):  
Epithelial Cell ◽  
Important Determinant ◽  
Alveolar Epithelial Cell ◽  
Surfactant Protein ◽  
Type I ◽  
Mrna Levels ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Lung Expansion ◽  
Birth Type

Basal lung expansion is an important determinant of alveolar epithelial cell (AEC) phenotype in the fetus. Because basal lung expansion increases toward term and is reduced after birth, we hypothesized that these changes would be associated with altered proportions of AECs. AEC proportions were calculated with electron microscopy in fetal and postnatal sheep. Type I AECs increased from 4.8 ± 1.3% at 91 days to 63.0 ± 3.6% at 111 days of gestation, remained at this level until term, and decreased to 44.8 ± 1.8% after birth. Type II AECs increased from 4.3 ± 1.5% at 111 days to 29.6 ± 4.1% at 128 days of gestation, remained at this level until term, and then increased to 52.9 ± 1.5% after birth. Surfactant protein (SP)-A, -B and -C mRNA levels increased with increasing gestational age before birth, but the changes in SP expression after birth were inconsistent. Thus before birth type I AECs predominate, whereas after birth type II AECs predominate, possibly due to the reduction in basal lung expansion associated with the entry of air into the lungs.

scholarly journals Differential Regulation of Gene Expression of Alveolar Epithelial Cell Markers in Human Lung Adenocarcinoma-Derived A549 Clones

2015 ◽  
Vol 2015 ◽  
pp. 1-20 ◽  
Author(s):  
Hiroshi Kondo ◽  
Keiko Miyoshi ◽  
Shoji Sakiyama ◽  
Akira Tangoku ◽  
Takafumi Noma
Keyword(s):  
Gene Expression ◽  
Epithelial Cell ◽  
Mapk Pathway ◽  
Alveolar Epithelial Cell ◽  
Marker Gene ◽  
Regulation Of Gene Expression ◽  
Surfactant Protein ◽  
Specific Gene ◽  
Expression Levels ◽  
Alveolar Epithelial

Stem cell therapy appears to be promising for restoring damaged or irreparable lung tissue. However, establishing a simple and reproducible protocol for preparing lung progenitor populations is difficult because the molecular basis for alveolar epithelial cell differentiation is not fully understood. We investigated anin vitrosystem to analyze the regulatory mechanisms of alveolus-specific gene expression using a human alveolar epithelial type II (ATII) cell line, A549. After cloning A549 subpopulations, each clone was classified into five groups according to cell morphology and marker gene expression. Two clones (B7 and H12) were further analyzed. Under serum-free culture conditions,surfactant protein C(SPC), an ATII marker, was upregulated in both H12 and B7.Aquaporin 5(AQP5), an ATI marker, was upregulated in H12 and significantly induced in B7. When the RAS/MAPK pathway was inhibited,SPCandthyroid transcription factor-1(TTF-1) expression levels were enhanced. After treatment with dexamethasone (DEX), 8-bromoadenosine 3′5′-cyclic monophosphate (8-Br-cAMP), 3-isobutyl-1-methylxanthine (IBMX), and keratinocyte growth factor (KGF),surfactant protein BandTTF-1expression levels were enhanced. We found that A549-derived clones have plasticity in gene expression of alveolar epithelial differentiation markers and could be useful in studying ATII maintenance and differentiation.

scholarly journals Human Alveolar Epithelial Cell Injury Induced by Cigarette Smoke

PLoS ONE ◽  
2011 ◽  
Vol 6 (12) ◽  
pp. e26059 ◽  
Author(s):  
Beata Kosmider ◽  
Elise M. Messier ◽  
Hong Wei Chu ◽  
Robert J. Mason
Keyword(s):  
Epithelial Cell ◽  
Cigarette Smoke ◽  
Cell Injury ◽  
Alveolar Epithelial Cell ◽  
Alveolar Epithelial ◽  
Human Alveolar Epithelial Cell ◽  
Epithelial Cell Injury

Effect of Steroids on the Synthesis of Complement C3 in a Human Alveolar Epithelial Cell Line

1993 ◽  
Vol 19 (5) ◽  
pp. 603-616 ◽  
Author(s):  
Terence L. Zach ◽  
Vicki A. Herrman ◽  
Laura D. Hill ◽  
M. Patricia Leuschen
Keyword(s):  
Epithelial Cell ◽  
Cell Line ◽  
Alveolar Epithelial Cell ◽  
Complement C3 ◽  
Epithelial Cell Line ◽  
Alveolar Epithelial ◽  
Human Alveolar Epithelial Cell

scholarly journals Role of collagenase in mediating in vitro alveolar epithelial wound repair

1999 ◽  
Vol 112 (2) ◽  
pp. 243-252
Author(s):  
E. Planus ◽  
S. Galiacy ◽  
M. Matthay ◽  
V. Laurent ◽  
J. Gavrilovic ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Adhesion ◽  
Epithelial Cell ◽  
Type I Collagen ◽  
Alveolar Epithelial Cell ◽  
Cell Monolayer ◽  
Type I ◽  
Type Ii ◽  
Alveolar Epithelial

Type II pneumocytes are essential for repair of the injured alveolar epithelium. The effect of two MMP collagenases, MMP-1 and MMP-13 on alveolar epithelial repair was studied in vitro. The A549 alveolar epithelial cell line and primary rat alveolar epithelial cell cultures were used. Cell adhesion and cell migration were measured with and without exogenous MMP-1. Wound healing of a cell monolayer of rat alveolar epithelial cell after a mechanical injury was evaluated by time lapse video analysis. Cell adhesion on type I collagen, as well as cytoskeleton stiffness, was decreased in the presence of exogenous collagenases. A similar decrease was observed when cell adhesion was tested on collagen that was first incubated with MMP-1 (versus control on intact collagen). Cell migration on type I collagen was promoted by collagenases. Wound healing of an alveolar epithelial cell monolayer was enhanced in the presence of exogenous collagenases. Our results suggest that collagenases could modulate the repair process by decreasing cell adhesion and cell stiffness, and by increasing cell migration on type I collagen. Collagen degradation could modify cell adhesion sites and collagen degradation peptides could induce alveolar type II pneumocyte migration. New insights regarding alveolar epithelial cell migration are particularly relevant to investigate early events during alveolar epithelial repair following lung injury.

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