ArticleJournal of Korean medical science2013
Expression of semaphorin 3A and neuropilin 1 in asthma.
Article in Journal of Korean medical science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 20 citations in OpenAlex.
- Serum neuropilin-1 level may predict airway remodeling based on age and smoking status in asthma.Asia Pacific allergy · 2025Article
- Semaphorin-3A: a promising therapeutic tool in allergic rhinitis.Immunologic research · 2022Review
- Article
- Perspectives and potential approaches for targeting neuropilin 1 in SARS-CoV-2 infection.Molecular medicine (Cambridge, Mass.) · 2021Review
- [The involvement of neuropilin-1 in primary immune thrombocytopenia].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2021Article
- The role of Neuropilin-1 in COVID-19.PLoS pathogens · 2021Review
- Semaphorin 3A: A Potential Target for Low Back Pain.Frontiers in aging neuroscience · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropilin 1 (NP1) is a part of essential receptor complexes mediating both semaphorin3A (SEMA3A) and vascular endothelial growth factor (VEGF) which is one of important mediators involved in the pathogenesis of asthma. Therefore, it is possible that SEMA3A plays a role in the pathogenesis of asthma through attenuation of VEGF-mediated effects. In the present study, we aimed to evaluate expression levels of SEMA3A and NP1 using induced sputum of asthmatics and a murine model of asthma. Firstly, SEMA3A and NP1 expressions in induced sputum of asthmatics and SEMA3A and NP1 expression on bronchoalveolar lavage (BAL) cells and lung homogenates of asthmatic mice were determined. Then we evaluated the immunolocalization of VEGF receptor 1 (VEGFR1), VEGF receptor 2 (VEGFR2), and NP1 expressions on asthmatic mice lung tissue and their subcellular distributions using fibroblast and BEAS2B cell lines. Sputum SEMA3A and NP1 expressions were significantly higher in asthmatics than controls. Similarly, SEMA3A and NP1 expressions on BAL cells and lung homogenates were significantly elevated in asthmatic mice compared to control mice. Immunohistochemical analysis showed that VEGFR1, VEGFR2, and NP1 expressions were also uniformly increased in asthmatic mice. Our observations suggest that SEMA3A and NP1 may play important roles in the pathogenesis of asthma.
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