ArticleBMC pulmonary medicine2015
Transgenically-expressed secretoglobin 3A2 accelerates resolution of bleomycin-induced pulmonary fibrosis in mice.
Article in BMC pulmonary medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Circulating SCGB3A2 Is Associated With Impaired Coronary Collateralization in Patients With Chronic Total Occlusion and Type 2 Diabetes: A Proteomic Discovery and Validation Study.Journal of diabetes · 2026Article
- Single-cell and spatial transcriptomics reveal a stress-induced EMT-like epithelial subset driving immune activation in silica-injured lung.Frontiers in immunology · 2025Article
- Secretoglobin 3A2 peptides have therapeutic potential for allergic airway inflammation.Life sciences · 2024Article
- Secretoglobin 3A2 protects lung from developing cigarette smoke-induced pulmonary emphysema.The international journal of biochemistry & cell biology · 2023Article
- Emerging role of an immunomodulatory protein secretoglobin 3A2 in human diseases.Pharmacology & therapeutics · 2022Review
- Development of Aging-Related Emphysematous and Lymphoma-Like Lesions is Enhanced by the Lack of Secretoglobin 3A2 in Mouse Lungs.International journal of chronic obstructive pulmonary disease · 2022Article
- Article
- Spatiotemporal Expression of Three Secretoglobin Proteins, SCGB1A1, SCGB3A1, and SCGB3A2, in Mouse Airway Epithelia.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019Article
- Local lung hypoxia determines epithelial fate decisions during alveolar regeneration.Nature cell biology · 2017Article
- Association Between Secretoglobin Family 3A Member 2 (SCGB3A2) Gene Polymorphisms and Asthma in a Korean Population.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- Deficiency of α7 nicotinic acetylcholine receptor attenuates bleomycin-induced lung fibrosis in mice.Molecular medicine (Cambridge, Mass.) · 2017Article
- Pediatric Acute Respiratory Distress Syndrome: Fibrosis versus Repair.Frontiers in pediatrics · 2016Review
- Secretoglobin Superfamily Protein SCGB3A2 Alleviates House Dust Mite-Induced Allergic Airway Inflammation in Mice.International archives of allergy and immunology · 2016Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundSecretoglobin (SCGB) 3A2, a cytokine-like secretory protein of small molecular weight, is predominantly expressed in airway epithelial cells. While SCGB3A2 is known to have anti-inflammatory, growth factor, and anti-fibrotic activities, whether SCGB3A2 has any other roles, particularly in lung homeostasis and disease has not been demonstrated in vivo. The aim of this study was to address these questions in mice.
methodsA transgenic mouse line that expresses SCGB3A2 in the lung using the human surfactant protein-C promoter was established. Detailed histological, immunohistochemical, physiological, and molecular characterization of the Scgb3a2-transgenic mouse lungs were carried out. Scgb3a2-transgenic and wild-type mice were subjected to bleomycin-induced pulmonary fibrosis model, and their lungs and bronchoalveolar lavage fluids were collected at various time points during 9 weeks post-bleomycin treatment for further analysis.
resultsAdult Scgb3a2-transgenic mouse lungs expressed approximately five-fold higher levels of SCGB3A2 protein in comparison to wild-type mice as determined by western blotting of lung tissues. Immunohistochemistry showed that expression was localized to alveolar type II cells in addition to airway epithelial cells, thus accurately reflecting the site of surfactant protein-C expression. Scgb3a2-transgenic mice showed normal lung development and histology, and no overt gross phenotypes. However, when subjected to a bleomycin-induced pulmonary fibrosis model, they initially exhibited exacerbated fibrosis at 3 weeks post-bleomycin administration that was more rapidly resolved by 6 weeks as compared with wild-type mice, as determined by lung histology, Masson Trichrome staining and hydroxyproline content, inflammatory cell numbers, expression of collagen genes, and proinflammatory cytokine levels. The decrease of fibrosis coincided with the increased expression of SCGB3A2 in Scgb3a2-transgenic lungs.
conclusionsThese results demonstrate that SCGB3A2 is an anti-fibrotic agent, and suggest a possible therapeutic use of recombinant SCGB3A2 in the treatment of pulmonary fibrosis.
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