Comprehensive characterisation of pulmonary and serum surfactant protein D in COPD

Winkler, Carla; Atochina‐Vasserman, Elena N.; Holz, Olaf; Beers, Michael F.; Erpenbeck, Veit J.; Krug, Norbert; Roepcke, Stefan; Lauer, Gereon; Elmlinger, Martin W.; Hohlfeld, Jens M.

doi:10.1186/1465-9921-12-29

Cited by 112 publications

(125 citation statements)

References 32 publications

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“…However, the ECLIPSE investigator failed to find a significant relationship between FEV1% predicted and SP-D in COPD patients [24]. In spite of that, our findings were in line with those of Sin et al [28] who showed an inverse correlation between circulating SP-D and FEV1 in COPD patients and those with Winkler et al [29], who found an inverse correlation of SP-D levels with FEV1/FVC in COPD. Consistently, we observed a positive correlation between serum SP-D with MDA and PC in patients with COPD.…”

Section: Discussionsupporting

confidence: 89%

Study of Role of Surfactant Protein-D, Malondialdehyde, Protein Carbonyl and its Correlation with Airflow Obstruction (FEV1% Predicted) in Patients with Smoker Chronic Obstructive Pulmonary Disease (COPD)

Pawar¹,

Abhang²

2017

Biochem Anal Biochem

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Section: Discussionsupporting

confidence: 89%

Study of Role of Surfactant Protein-D, Malondialdehyde, Protein Carbonyl and its Correlation with Airflow Obstruction (FEV1% Predicted) in Patients with Smoker Chronic Obstructive Pulmonary Disease (COPD)

Pawar¹,

Abhang²

2017

Biochem Anal Biochem

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“…Reminiscent of findings in this study, targeted deletion of the pulmonary collectins SP-A and SP-D has been shown to promote airway inflammation (1,34) by enhancing alveolar macrophage activation (10,15). Interestingly, the type of immune modulatory response induced by these proteins is influenced by the binding orientation of SP-A or SP-D on alveolar macrophages.…”

Section: Discussionsupporting

confidence: 65%

C1q Deficiency Promotes Pulmonary Vascular Inflammation and Enhances the Susceptibility of the Lung Endothelium to Injury

Shah

Romero

Zhu

et al. 2015

Journal of Biological Chemistry

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The collectin proteins are innate immune molecules found in high concentrations on the epithelial and endothelial surfaces of the lung. While these proteins are known to have important anti-inflammatory actions in the airways of the lung little is known of their functional importance in the pulmonary circulation. We recently demonstrated that the circulating collectin protein adiponectin has potent anti-inflammatory effects on the lung endothelium, leading us to reason that other structurally related proteins might have similar effects. To test this hypothesis, we investigated the anti-inflammatory actions of C1q in lung endothelial homeostasis and the pulmonary vascular response to LPS or HCl injury. We show that lung endothelium from C1q-deficient (C1q ؊/؊ ) mice expresses higher baseline levels of the vascular adhesion markers ICAM-1, VCAM-1, and E-selectin when compared with wild-type mice. Further, we demonstrate that these changes are associated with enhanced susceptibility of the lung to injury as evident by increased expression of adhesion markers, enhanced production of proinflammatory cytokines, and augmented neutrophil recruitment. Additionally, we found that C1q ؊/؊ mice also exhibited enhanced endothelial barrier dysfunction after injury as manifested by decreased expression of junctional adherens proteins and enhanced vascular leakage. Mechanistically, C1q appears to mediate its effects by inhibiting phosphorylation of p38 mitogen-activated protein kinase (MAPK) and blocking nuclear translocation of the P65 subunit of nuclear factor (NF)-B. In summary, our findings indicate a previously unrecognized role for C1q in pulmonary vascular homeostasis and provide added support for the hypothesis that circulating collectin proteins have protective effects on the lung endothelium.

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“…In addition, a significant positive correlation was observed between BALF SP-D levels and respiratory function (FEV 1 /FVC). 26,28) In our study, stimulation of PPARβ/δ by GW0742 increased the expression of SP-D in lung tissue and improved FEV 0.05/FVC in emphysema model mice.…”

Section: Discussionsupporting

confidence: 55%

Pulmonary Administration of GW0742, a High-Affinity Peroxisome Proliferator-Activated Receptor Agonist, Repairs Collapsed Alveoli in an Elastase-Induced Mouse Model of Emphysema

Ozawa

Horiguchi

Akita

et al. 2016

Biological & Pharmaceutical Bulletin

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Pulmonary emphysema is a disease in which lung alveoli are irreversibly damaged, thus compromising lung function. Our previous study revealed that all-trans-retinoic acid (ATRA) induces the differentiation of human lung alveolar epithelial type 2 progenitor cells and repairs the alveoli of emphysema model mice. ATRA also reportedly has the ability to activate peroxisome proliferator-activated receptor (PPAR) β/δ. A selective PPARβ/δ ligand has been reported to induce the differentiation of human keratinocytes during wound repair. Here, we demonstrate that treatment using a high-affinity PPARβ/δ agonist, GW0742, reverses the lung tissue damage induced by elastase in emphysema-model mice and improves respiratory function. Mice treated with elastase, which collapsed their alveoli, were then treated with either 10% dimethyl sulfoxide (DMSO) in saline (control group) or GW0742 (1.0 mg/kg twice a week) by pulmonary administration. Treatment with GW0742 for 2 weeks increased the in vivo expression of surfactant proteins A and D, which are known alveolar type II epithelial cell markers. GW0742 treatment also shortened the average distance between alveolar walls in the lungs of emphysema model mice, compared with a control group treated with 10% DMSO in saline. Treatment with GW0742 for 3 weeks also improved tissue elastance (cm H 2 O/mL), as well as the ratio of the forced expiratory volume in the first 0.05 s to the forced vital capacity (FEV 0.05/ FVC). In each of these experiments, GW0742 treatment reversed the damage caused by elastase. In conclusion, PPARβ/δ agonists are potential therapeutic agents for pulmonary emphysema.

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Comprehensive characterisation of pulmonary and serum surfactant protein D in COPD

Cited by 112 publications

References 32 publications

Study of Role of Surfactant Protein-D, Malondialdehyde, Protein Carbonyl and its Correlation with Airflow Obstruction (FEV1% Predicted) in Patients with Smoker Chronic Obstructive Pulmonary Disease (COPD)

Study of Role of Surfactant Protein-D, Malondialdehyde, Protein Carbonyl and its Correlation with Airflow Obstruction (FEV1% Predicted) in Patients with Smoker Chronic Obstructive Pulmonary Disease (COPD)

C1q Deficiency Promotes Pulmonary Vascular Inflammation and Enhances the Susceptibility of the Lung Endothelium to Injury

Pulmonary Administration of GW0742, a High-Affinity Peroxisome Proliferator-Activated Receptor Agonist, Repairs Collapsed Alveoli in an Elastase-Induced Mouse Model of Emphysema

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