Ox-LDL-induced TGF-β1 production in human alveolar epithelial cells: Involvement of the Ras/ERK/PLTP pathway

2012 ◽  
Vol 227 (9) ◽  
pp. 3185-3191 ◽  
Author(s):  
Ling-Li Guo ◽  
Ya-Juan Chen ◽  
Tao Wang ◽  
Jing An ◽  
Cheng-Na Wang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Alveolar Epithelial Cells ◽  
Alveolar Epithelial ◽  
Tgf Β1 ◽  
Human Alveolar Epithelial Cells

scholarly journals CXCL9 Regulates TGF-β1–Induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells

2015 ◽  
Vol 195 (6) ◽  
pp. 2788-2796 ◽  
Author(s):  
Sarah L. O’Beirne ◽  
Sinead M. Walsh ◽  
Aurélie Fabre ◽  
Carlota Reviriego ◽  
Julie C. Worrell ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Alveolar Epithelial Cells ◽  
Mesenchymal Transition ◽  
Alveolar Epithelial ◽  
Tgf Β1 ◽  
Human Alveolar Epithelial Cells

Resolvin E1 Improves Mitochondrial Function in Human Alveolar Epithelial Cells during Severe Inflammation

Lipids ◽  
2019 ◽  
Vol 54 (1) ◽  
pp. 53-65 ◽  
Author(s):  
Konstantin Mayer ◽  
Natascha Sommer ◽  
Karl Hache ◽  
Andreas Hecker ◽  
Sylvia Reiche ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mitochondrial Function ◽  
Alveolar Epithelial Cells ◽  
Alveolar Epithelial ◽  
Severe Inflammation ◽  
Human Alveolar Epithelial Cells

Cellular Toxicity of Various Inhalable Metal Nanoparticles on Human Alveolar Epithelial Cells

2007 ◽  
Vol 19 (sup1) ◽  
pp. 59-65 ◽  
Author(s):  
Seoyoung Park ◽  
Yong Kwon Lee ◽  
Moonju Jung ◽  
Ki Heon Kim ◽  
Namhyun Chung ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Metal Nanoparticles ◽  
Alveolar Epithelial Cells ◽  
Cellular Toxicity ◽  
Alveolar Epithelial ◽  
Human Alveolar Epithelial Cells

scholarly journals CCR2 and CXCR3 agonistic chemokines are differently expressed and regulated in human alveolar epithelial cells type II

2005 ◽  
Vol 6 (1) ◽  
Author(s):  
Dmitri V Pechkovsky ◽  
Torsten Goldmann ◽  
Corinna Ludwig ◽  
Antje Prasse ◽  
Ekkehard Vollmer ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Alveolar Epithelial Cells ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Human Alveolar Epithelial Cells

Nitric oxide attenuates epithelial-mesenchymal transition in alveolar epithelial cells

2007 ◽  
Vol 293 (1) ◽  
pp. L212-L221 ◽  
Author(s):  
Shilpa Vyas-Read ◽  
Philip W. Shaul ◽  
Ivan S. Yuhanna ◽  
Brigham C. Willis
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Epithelial Cells ◽  
Epithelial Mesenchymal Transition ◽  
Alveolar Epithelial Cells ◽  
No Production ◽  
Mesenchymal Transition ◽  
Alveolar Epithelial ◽  
Oxide Synthase ◽  
Tgf Β1

Patients with interstitial lung diseases, such as idiopathic pulmonary fibrosis (IPF) and bronchopulmonary dysplasia (BPD), suffer from lung fibrosis secondary to myofibroblast-mediated excessive ECM deposition and destruction of lung architecture. Transforming growth factor (TGF)-β1 induces epithelial-mesenchymal transition (EMT) of alveolar epithelial cells (AEC) to myofibroblasts both in vitro and in vivo. Inhaled nitric oxide (NO) attenuates ECM accumulation, enhances lung growth, and decreases alveolar myofibroblast number in experimental models. We therefore hypothesized that NO attenuates TGF-β1-induced EMT in cultured AEC. Studies of the capacity for endogenous NO production in AEC revealed that endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) are expressed and active in AEC. Total NOS activity was 1.3 pmol·mg protein−1·min−1 with 67% derived from eNOS. TGF-β1 (50 pM) suppressed eNOS expression by more than 60% and activity by 83% but did not affect iNOS expression or activity. Inhibition of endogenous NOS with l-NAME led to spontaneous EMT, manifested by increased α-smooth muscle actin (α-SMA) expression and a fibroblast-like morphology. Provision of exogenous NO to TGF-β1-treated AEC decreased stress fiber-associated α-SMA expression and decreased collagen I expression by 80%. NO-treated AEC also retained an epithelial morphology and expressed increased lamellar protein, E-cadherin, and pro-surfactant protein B compared with those treated with TGF-β alone. These findings indicate that NO serves a critical role in preserving an epithelial phenotype and in attenuating EMT in AEC. NO-mediated regulation of AEC fate may have important implications in the pathophysiology and treatment of diseases such as IPF and BPD.

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