scholarly journals Transverse relaxation rates of pulmonary dissolved‐phase Hyperpolarized 129 Xe as a biomarker of lung injury in idiopathic pulmonary fibrosis

2020 ◽  
Vol 84 (4) ◽  
pp. 1857-1867
Author(s):  
Jeff Kammerman ◽  
Andrew D. Hahn ◽  
Robert V. Cadman ◽  
Annelise Malkus ◽  
David Mummy ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Lung Injury ◽  
Relaxation Rates ◽  
Transverse Relaxation ◽  
Dissolved Phase

New IL-1 family IL-38 is highly expressed in alveolar cells of drug-induced lung injury and idiopathic pulmonary fibrosis

2016 ◽  
Author(s):  
Masaki Tominaga ◽  
Masaki Okamoto ◽  
Takashi Kinoshita ◽  
Yuki Sakazaki ◽  
Masanobu Matsuoka ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Lung Injury ◽  
Alveolar Cells ◽  
Drug Induced

Inhibition of Wnt/β-catenin signaling promotes epithelial differentiation of mesenchymal stem cells and repairs bleomycin-induced lung injury

2014 ◽  
Vol 307 (3) ◽  
pp. C234-C244 ◽  
Author(s):  
Cong Wang ◽  
Huiming Zhu ◽  
Zhaorui Sun ◽  
Zou Xiang ◽  
Yuanyuan Ge ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Lung Injury ◽  
Signaling Pathway ◽  
Epithelial Differentiation ◽  
Unknown Etiology ◽  
Alveolar Type ◽  
Coculture System

Idiopathic pulmonary fibrosis is a progressive lung disorder of unknown etiology. Previous studies have shown that aberrant activation of the Wnt/β-catenin signaling cascade occurs in lungs of patients with idiopathic pulmonary fibrosis. Given the important roles of the Wnt/β-catenin signaling pathway in the development of pulmonary fibrosis, we targeted this pathway for the intervention of pulmonary fibrosis with XAV939, a small molecule that specifically inhibits Tankyrase 1/2, eventually leading to the degradation of β-catenin and suppression of the Wnt/β-catenin signaling pathway. Our results demonstrated that XAV939 significantly inhibited the activation of Wnt/β-catenin signaling and attenuated bleomycin-induced lung fibrosis in mice, and thus improved the survival of mice with lung injury. Interestingly, previous investigations have confirmed that endogenous and exogenous mesenchymal stem cells could be recruited to the injured lung, although the exact effects of these cells are debatable. To determine the effect of Wnt/β-catenin signaling in the epithelial differentiation of bone marrow-derived mesenchymal stem cells (BM-MSCs), we established a coculture system that contains BM-MSCs and alveolar type II epithelial cells. The in vitro experiments demonstrated that XAV939 could promote the differentiation of BM-MSCs into an epithelium-like phenotype in the coculture system. We also found that XAV939 could inhibit the proliferation and myofibroblast differentiation of NIH/3T3 fibroblasts. This work supports that inhibition of the Wnt/β-catenin signaling pathway may be exploited for the treatment of idiopathic pulmonary fibrosis for which effective treatment strategies are still lacking.

Pathogenesis pathways of idiopathic pulmonary fibrosis in bleomycin-induced lung injury model in mice

2014 ◽  
Vol 190 ◽  
pp. 113-117 ◽  
Author(s):  
Keyun Shi ◽  
Jianzhong Jiang ◽  
Tieliang Ma ◽  
Jing Xie ◽  
Lirong Duan ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Lung Injury ◽  
Injury Model ◽  
Lung Injury Model

scholarly journals Plasma biomarker profiles in acute exacerbation of idiopathic pulmonary fibrosis

2010 ◽  
Vol 299 (1) ◽  
pp. L3-L7 ◽  
Author(s):  
Harold R. Collard ◽  
Carolyn S. Calfee ◽  
Paul J. Wolters ◽  
Jin Woo Song ◽  
Sang-Bum Hong ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Lung Injury ◽  
Acute Exacerbation ◽  
Cell Injury ◽  
Surfactant Protein D ◽  
Type Ii ◽  
Plasma Biomarker ◽  
Alveolar Epithelial

Little is known about the pathobiology of acute exacerbation of idiopathic pulmonary fibrosis (IPF), a condition that shares clinical and histopathological features with acute lung injury. Plasma biomarkers have been well studied in acute lung injury and have provided insight into the underlying disease mechanism. The objective of this study was to determine the plasma biomarker profile of acute exacerbation of IPF and compare this profile with that of stable IPF and acute lung injury. Plasma was collected from patients with stable IPF, acute exacerbation of IPF, and acute lung injury for measurement of biomarkers of cellular activity/injury (receptor for advanced glycation endproducts, surfactant protein D, KL-6, von Willebrand factor), systemic inflammation (IL-6), and coagulation/fibrinolysis (protein C, thrombomodulin, plasminogen activator inhibitor-1). Plasma from patients with acute exacerbation of IPF showed significant elevations in markers of type II alveolar epithelial cell injury and/or proliferation, endothelial cell injury, and coagulation. This profile differed from the biomarker profile in patients with acute lung injury. These findings support the hypothesis that type II alveolar epithelial cells are centrally involved in the pathobiology of acute exacerbation of IPF. Furthermore, they suggest that acute exacerbation of IPF has a distinct plasma biomarker profile from that of acute lung injury.

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