scholarly journals P109 Circulating MMP Activity and Lung Remodelling in LAM

Thorax ◽  
2012 ◽  
Vol 67 (Suppl 2) ◽  
pp. A110.1-A110
Author(s):  
JL Cane ◽  
WY Chang ◽  
R Gallagher ◽  
V Gontu ◽  
M Kumaran ◽  
...  
Keyword(s):  
Lung Remodelling

The role of surfactant protein D in fibrotic lung remodelling

Pneumologie ◽  
2014 ◽  
Vol 68 (06) ◽  
Author(s):  
J Viereck ◽  
L Knudsen ◽  
JP Schneider ◽  
M Ochs ◽  
T Thum
Keyword(s):  
Surfactant Protein ◽  
Surfactant Protein D ◽  
Lung Remodelling

Modification of the pulmonary renin–angiotensin system and lung structural remodelling in congestive heart failure

2006 ◽  
Vol 111 (3) ◽  
pp. 217-224 ◽  
Author(s):  
Frederic Lefebvre ◽  
Annick Préfontaine ◽  
Angelino Calderone ◽  
Alexandre Caron ◽  
Jean-François Jasmin ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Renin Angiotensin System ◽  
At1 Receptor ◽  
Receptor Expression ◽  
Coronary Artery Ligation ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Lung Remodelling

Lung structural remodelling, characterized by myofibroblast proliferation and collagen deposition, contributes to impaired functional capacity in CHF (congestive heart failure). As the lung is the primary site for the formation of Ang II (angiotensin II), local modifications of this system could contribute to lung remodelling. Rats with CHF, induced following myocardial infarction (MI) via coronary artery ligation, were compared with sham-operated controls. The MI group developed lung remodelling as confirmed by morphometric measurements and immunohistochemistry. Pulmonary Ang II concentrations increased more than 6-fold (P<0.01), and AT1 (Ang II type 1) receptor expression was elevated by 3-fold (P<0.01) with evidence of distribution in myofibroblasts. AT2 (Ang II type 2) receptor expression was unchanged. In isolated lung myofibroblasts, AT1 and AT2 receptors were expressed, and Ang II stimulated proliferation as measured by [3H]thymidine incorporation. In normal rats, chronic intravenous infusion of Ang II (0.5 mg·kg−1 of body weight·day−1) for 28 days significantly increased mean arterial pressure (P<0.05), without pulmonary hypertension, lung remodelling or a change in AT1 receptor expression. We conclude that there is a modification of the pulmonary renin–angiotensin system in CHF, with increased Ang II levels and AT1 receptor expression on myofibroblasts. Although this may contribute to lung remodelling, the lack of effect of increased plasma Ang II levels alone suggests the importance of local pulmonary Ang II levels combined with the effect of other factors activated in CHF.

Bone marrow-derived progenitor cells contribute to lung remodelling after myocardial infarction

2007 ◽  
Vol 16 (6) ◽  
pp. 321-328 ◽  
Author(s):  
Jocelyn Dupuis ◽  
Annick Préfontaine ◽  
Louis Villeneuve ◽  
Nathalie Ruel ◽  
Frédéric Lefebvre ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Bone Marrow ◽  
Progenitor Cells ◽  
Lung Remodelling

scholarly journals Regional distribution of high-attenuation areas on chest computed tomography in the Multi-Ethnic Study of Atherosclerosis

2020 ◽  
Vol 6 (1) ◽  
pp. 00115-2019 ◽  
Author(s):  
Bina Choi ◽  
Steven M. Kawut ◽  
Ganesh Raghu ◽  
Eric Hoffman ◽  
Russell Tracy ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Regional Distribution ◽  
Hazard Ratio ◽  
Ethnic Study ◽  
High Attenuation ◽  
Mortality Hazard ◽  
All Cause Mortality ◽  
Specific Mortality ◽  
Mortality Hazard Ratio ◽  
Lung Remodelling

High-attenuation areas (HAA) are a computed tomography-based quantitative measure of subclinical interstitial lung disease (ILD). We aimed to validate HAA in lung regions that are less subject to artefacts, such as extravascular lung water or dependent atelectasis. We examined the associations of HAA within six lung regions (basilar, non-basilar, peel, core, basilar peel, basilar core) with serum biomarkers of lung remodelling, forced vital capacity (FVC), visually-assessed interstitial lung abnormalities (ILA), and all-cause and ILD-specific mortality.We performed cross-sectional and longitudinal analyses of participants in the Multi-Ethnic Study of Atherosclerosis, a prospective cohort of 6814 adults aged 45–84 years without known cardiovascular disease who underwent cardiac computed tomography.Median regional HAA ranged from 3.8% in the peel to 4.8% in the basilar core. Doubling of regional HAA was associated with greater serum matrix metalloproteinase-7 (range 3.8% to 10.3%; p≤0.01), higher odds of ILA (OR 1.42 to 2.20; p≤0.03), and a higher risk of all-cause mortality (hazard ratio 1.20 to 1.47; p≤0.001). Doubling of regional HAA was associated with greater serum interleukin-6 (4.9% to 10.3%; p≤0.005) and higher risk of ILD-specific mortality (hazard ratio 3.30 to 3.98; p<0.001), except in the basilar core. Doubling of regional HAA was associated with lower FVC in the non-basilar, core and basilar core (113 mL to 186 mL; p<0.001).Associations of HAA with lung remodelling biomarkers, ILA risk and all-cause mortality were consistent across all regions of the lung, including dependent areas where atelectasis may be present. These findings support the validity of HAA as a measure of pathologic subclinical ILD.

Role of endothelin receptors on basal and endothelin-1-stimulated lung myofibroblast proliferationThis article is one of a selection of papers published in the special issue (part 1 of 2) on Forefronts in Endothelin.

2008 ◽  
Vol 86 (6) ◽  
pp. 337-342 ◽  
Author(s):  
Annick Préfontaine ◽  
Angelino Calderone ◽  
Jocelyn Dupuis
Keyword(s):  
Protein Synthesis ◽  
Confocal Imaging ◽  
Receptor Expression ◽  
Leucine Incorporation ◽  
Endothelin 1 ◽  
Selective Blockade ◽  
Dual Blockade ◽  
Lung Remodelling ◽  
Selection Of

Proliferation of myofibroblasts (MYF) contributes to numerous lung disorders. Endothelin-1 (ET-1) production is increased in various lung diseases and could contribute to lung remodelling. The respective roles of ETA and ETB receptors (ETA-R, ETB-R) and the role of endogenous ET-1 production by lung MYF on proliferation of MYF remain uncertain. Rat lung MYF were isolated and 3H-thymidine and 3H-leucine incorporation assays were completed in the presence of a selective ETA-R antagonist, a selective ETB-R antagonist, or a combination of both. Receptor expression was evaluated by confocal imaging, and ET-1 levels were measured by ELISA. Confocal microscopy revealed abundant ETA-R and ETB-R expression on lung MYF. ET-1 (10 nmol/L) stimulated MYF proliferation and protein synthesis through PI3-kinase and p38 pathways. Although neither selective ETA-R blockade (BQ-123, 1 μmol/L) nor selective ETB-R blockade (BQ-788, 1 μmol/L) alone inhibited proliferation or protein synthesis, their combination almost completely abolished ET-1 mitogenic effect. Surprisingly, basal MYF proliferation was increased by selective blockade of either ETA-R or ETB-R alone, but not by dual blockade. ET-1 levels were not affected by the antagonists. Our findings indicate that both the ETA-R and the ETB-R regulate basal and stimulated lung MYF proliferation and suggest possible interactions between the receptors.

scholarly journals Targeting of cathepsin S reduces cystic fibrosis-like lung disease

2019 ◽  
Vol 53 (3) ◽  
pp. 1801523 ◽  
Author(s):  
Donna M. Small ◽  
Ryan R. Brown ◽  
Declan F. Doherty ◽  
Anthony Abladey ◽  
Zhe Zhou-Suckow ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Lung Disease ◽  
Pulmonary Inflammation ◽  
Lung Damage ◽  
Cathepsin S ◽  
Lung Pathology ◽  
Wild Type ◽  
Mucin Expression ◽  
Protease Activated Receptor 2 ◽  
Lung Remodelling

Cathepsin S (CatS) is upregulated in the lungs of patients with cystic fibrosis (CF). However, its role in CF lung disease pathogenesis remains unclear.In this study, β-epithelial Na+ channel-overexpressing transgenic (βENaC-Tg) mice, a model of CF-like lung disease, were crossed with CatS null (CatS−/−) mice or treated with the CatS inhibitor VBY-999.Levels of active CatS were elevated in the lungs of βENaC-Tg mice compared with wild-type (WT) littermates. CatS−/−βENaC-Tg mice exhibited decreased pulmonary inflammation, mucus obstruction and structural lung damage compared with βENaC-Tg mice. Pharmacological inhibition of CatS resulted in a significant decrease in pulmonary inflammation, lung damage and mucus plugging in the lungs of βENaC-Tg mice. In addition, instillation of CatS into the lungs of WT mice resulted in inflammation, lung remodelling and upregulation of mucin expression. Inhibition of the CatS target, protease-activated receptor 2 (PAR2), in βENaC-Tg mice resulted in a reduction in airway inflammation and mucin expression, indicating a role for this receptor in CatS-induced lung pathology.Our data indicate an important role for CatS in the pathogenesis of CF-like lung disease mediated in part by PAR2 and highlight CatS as a therapeutic target.

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