scholarly journals Hyperoxia alters the mechanical properties of alveolar epithelial cells

2012 ◽  
Vol 302 (12) ◽  
pp. L1235-L1241 ◽  
Author(s):  
Esra Roan ◽  
Kristina Wilhelm ◽  
Alex Bada ◽  
Patrudu S. Makena ◽  
Vijay K. Gorantla ◽  
...  
Keyword(s):  
Mechanical Properties ◽  
Mechanical Ventilation ◽  
Elastic Modulus ◽  
Epithelial Cells ◽  
Lung Injury ◽  
Alveolar Epithelial Cells ◽  
Cyclic Stretch ◽  
Cell Deformability ◽  
Element Analysis ◽  
Alveolar Epithelial

Patients with severe acute lung injury are frequently administered high concentrations of oxygen (>50%) during mechanical ventilation. Long-term exposure to high levels of oxygen can cause lung injury in the absence of mechanical ventilation, but the combination of the two accelerates and increases injury. Hyperoxia causes injury to cells through the generation of excessive reactive oxygen species. However, the precise mechanisms that lead to epithelial injury and the reasons for increased injury caused by mechanical ventilation are not well understood. We hypothesized that alveolar epithelial cells (AECs) may be more susceptible to injury caused by mechanical ventilation if hyperoxia alters the mechanical properties of the cells causing them to resist deformation. To test this hypothesis, we used atomic force microscopy in the indentation mode to measure the mechanical properties of cultured AECs. Exposure of AECs to hyperoxia for 24 to 48 h caused a significant increase in the elastic modulus (a measure of resistance to deformation) of both primary rat type II AECs and a cell line of mouse AECs (MLE-12). Hyperoxia also caused remodeling of both actin and microtubules. The increase in elastic modulus was blocked by treatment with cytochalasin D. Using finite element analysis, we showed that the increase in elastic modulus can lead to increased stress near the cell perimeter in the presence of stretch. We then demonstrated that cyclic stretch of hyperoxia-treated cells caused significant cell detachment. Our results suggest that exposure to hyperoxia causes structural remodeling of AECs that leads to decreased cell deformability.

Human induced pluripotent stem cell–derived lung progenitor and alveolar epithelial cells attenuate hyperoxia-induced lung injury

Cytotherapy ◽  
2018 ◽  
Vol 20 (1) ◽  
pp. 108-125 ◽  
Author(s):  
Mehdi Shafa ◽  
Lavinia Iuliana Ionescu ◽  
Arul Vadivel ◽  
Jennifer J.P. Collins ◽  
Liqun Xu ◽  
...  
Keyword(s):  
Stem Cell ◽  
Epithelial Cells ◽  
Lung Injury ◽  
Pluripotent Stem Cell ◽  
Induced Pluripotent Stem Cell ◽  
Alveolar Epithelial Cells ◽  
Alveolar Epithelial ◽  
Induced Pluripotent ◽  
Lung Progenitor

scholarly journals Photobiomodulation prevents DNA fragmentation of alveolar epithelial cells and alters the mRNA levels of caspase 3 and Bcl-2 genes in acute lung injury

2018 ◽  
Vol 17 (7) ◽  
pp. 975-983 ◽  
Author(s):  
Luiz Philippe da Silva Sergio ◽  
Andrezza Maria Côrtes Thomé ◽  
Larissa Alexsandra da Silva Neto Trajano ◽  
Andre Luiz Mencalha ◽  
Adenilson de Souza da Fonseca ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Epithelial Cells ◽  
Lung Injury ◽  
Dna Fragmentation ◽  
Caspase 3 ◽  
Alveolar Epithelial Cells ◽  
Mrna Levels ◽  
Alveolar Epithelial ◽  
Life Threatening ◽  
Pulmonary Permeability

Acute lung injury (ALI) is defined as hyperinflammation that could occur from sepsis and lead to pulmonary permeability and edema, making them life-threatening diseases.

scholarly journals Overexpression of Sphingosine Kinase-1 and Sphingosine-1-Phosphate Receptor-3 in Severe Plasmodium falciparum Malaria with Pulmonary Edema

2020 ◽  
Vol 2020 ◽  
pp. 1-7 ◽  
Author(s):  
Parnpen Viriyavejakul ◽  
Chuchard Punsawad
Keyword(s):  
Plasmodium Falciparum ◽  
Epithelial Cells ◽  
Lung Injury ◽  
Pulmonary Edema ◽  
Sphingosine Kinase ◽  
Alveolar Epithelial Cells ◽  
Sphingosine Kinase 1 ◽  
Expression Levels ◽  
Alveolar Epithelial ◽  
Sphingosine 1 Phosphate

Pulmonary edema (PE) is a major cause of pulmonary manifestations of severe Plasmodium falciparum malaria and is usually associated with acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). The sphingosine kinase-1 (SphK-1)/sphingosine-1-phosphate receptor-3 (S1PR-3) pathway has recently been reported to affect the pathogenesis of lung injury, but the expression of these proteins in the lungs of severe P. falciparum malaria patients has not been investigated. The cellular expression of SphK-1 and S1PR-3 in lung tissues from autopsied patients with P. falciparum malaria was investigated using immunohistochemistry (IHC). Lung tissues from patients who died of severe P. falciparum malaria were classified into two groups based on histopathological findings: those with PE (18 patients) and those without PE (non-PE, 19 patients). Ten samples of normal lung tissues were used as the control group. The protein expression levels of SphK-1 and S1PR-3 were significantly upregulated in endothelial cells (ECs), alveolar epithelial cells, and alveolar macrophages (AMs) in the lungs of severe P. falciparum malaria patients with PE compared to those in the non-PE and control groups (all p<0.001). In addition, the SphK-1 and S1PR-3 expression levels were significantly positively correlated in pulmonary ECs (rs=0.922, p<0.001), alveolar epithelial cells (rs=0.995, p<0.001), and AMs (rs=0.969, p<0.001). In conclusion, both the SphK-1 and S1PR-3 proteins were overexpressed in the lung tissues of severe P. falciparum malaria patients with PE, suggesting that SphK-1 and S1PR-3 mediate the pathogenesis of PE in severe malaria. Targeting the regulation of SphK-1 and/or S1PR-3 may be an approach to treat pulmonary complications in severe P. falciparum patients.

scholarly journals Adipose Tissue-Derived Stem Cells Have the Ability to Differentiate into Alveolar Epithelial Cells and Ameliorate Lung Injury Caused by Elastase-Induced Emphysema in Mice

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Eriko Fukui ◽  
Soichiro Funaki ◽  
Kenji Kimura ◽  
Toru Momozane ◽  
Atsuomi Kimura ◽  
...  
Keyword(s):  
Stem Cells ◽  
Adipose Tissue ◽  
Epithelial Cells ◽  
Lung Injury ◽  
Alveolar Epithelial Cells ◽  
Chronic Obstructive ◽  
Alveolar Cells ◽  
Alveolar Epithelial

Chronic obstructive pulmonary disease is a leading cause of mortality globally, with no effective therapy yet established. Adipose tissue-derived stem cells (ADSCs) are useful for ameliorating lung injury in animal models. However, whether ADSCs differentiate into functional cells remains uncertain, and no study has reported on the mechanism by which ADSCs improve lung functionality. Thus, in this study, we examined whether ADSCs differentiate into lung alveolar cells and are able to ameliorate lung injury caused by elastase-induced emphysema in model mice. Here, we induced ADSCs to differentiate into type 2 alveolar epithelial cells in vitro. We demonstrated that ADSCs can differentiate into type 2 alveolar epithelial cells in an elastase-induced emphysematous lung and that ADSCs improve pulmonary function of emphysema model mice, as determined with spirometry and 129Xe MRI. These data revealed a novel function for ADSCs in promoting repair of the damaged lung by direct differentiation into alveolar epithelial cells.

Alveolar epithelial cells express both plasminogen activator and tissue factor. Potential role in repair of lung injury

CHEST Journal ◽  
1991 ◽  
Vol 99 (3) ◽  
pp. 25S-27 ◽  
Author(s):  
B. C. Marshall ◽  
B. R. Brown ◽  
M. A. Rothstein ◽  
N. V. Rao ◽  
J. R. Hoidal ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Lung Injury ◽  
Tissue Factor ◽  
Plasminogen Activator ◽  
Potential Role ◽  
Alveolar Epithelial Cells ◽  
Alveolar Epithelial
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