Observational studyMedicine2020
Surfactant protein A expression and distribution in human lung samples from smokers with or without chronic obstructive pulmonary disease in China.
Observational study in Medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Molecular Impact of Conventional and Electronic Cigarettes on Pulmonary Surfactant.International journal of molecular sciences · 2023Review
- Multiomics links global surfactant dysregulation with airflow obstruction and emphysema in COPD.ERJ open research · 2023Article
- Lipid-Protein and Protein-Protein Interactions in the Pulmonary Surfactant System and Their Role in Lung Homeostasis.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cigarette smoking is considered the main risk factor for chronic obstructive pulmonary disease (COPD), although the mechanism remains unknown. surfactant protein A (SP-A) is thought to protect the lung from smoking-induced damage, but related studies performed in China are scarce. The aim of the study is to assess alterations of SP-A expression and distribution in lung samples from Chinese smokers with or without COPD.This cross-sectional study assessed 45 men in Wuhan Tongji Hospital after lobectomy for lung cancer in June 2010 to September 2010. Peripheral lung specimens were collected from control nonsmokers without airflow obstruction (nonsmoking group, n = 15), smokers without airflow obstruction (smoking group, n = 15), and patients with COPD (COPD group, n = 15). SP-A expression levels in lung tissue samples and its distribution in lung cells, type II pneumocytes (PNII), and alveolar macrophages (MACR) were determined by immunoblotting and immunohistochemistry.SP-A levels were significantly decreased in the COPD group (1.00 ± 0.25) compared with the smoking (2.31 ± 0.64) and nonsmoking (8.03 ± 2.80) groups; the smoking group also showed significantly reduced levels compared with the nonsmoking group (P < .05). PNII expressing SP-A were less abundant in the COPD group (39.3% ± 7.1%) compared with the smoking group (76.2% ± 29.8%), whereas SP-A MACR were more abundant (92.4% ± 7.1% vs 68.5% ± 20.2%) (all P < .05). Among the 30 smokers, forced expiratory volume in one second (% predicted) was positively correlated with SP-A levels (r = 0.739) and the rate of SP-A+ PNII (r = 0.811), and negatively correlated with the rate of SP-A+ MACR (r = -0.758) (all P < .05).Changes in SP-A expression and distribution in lung tissues may be involved in COPD pathogenesis in smokers.
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