Expression of Semaphorin 3A and Neuropilin 1 in Asthma.
10.3346/jkms.2013.28.10.1435
- Author:
Eun Jin SHIM
1
;
Eunyoung CHUN
;
Hae Ryun KANG
;
Sang Heon CHO
;
Kyung Up MIN
;
Heung Woo PARK
Author Information
1. Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea. guinea71@snu.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Asthma;
Neuropilin;
Semaphorin-3A (SEMA3A);
Vascular Endothelial Growth Factor
- MeSH:
Animals;
Asthma/metabolism/pathology/*physiopathology;
Bronchoalveolar Lavage Fluid/cytology;
Cell Line;
Disease Models, Animal;
Female;
Fibroblasts/metabolism;
*Gene Expression Regulation;
Immunohistochemistry;
Lung/metabolism;
Male;
Mice;
Mice, Inbred C57BL;
Neuropilin-1/*genetics/metabolism;
Semaphorin-3A/*genetics/metabolism;
Sputum/metabolism;
Vascular Endothelial Growth Factor Receptor-1/metabolism;
Vascular Endothelial Growth Factor Receptor-2/metabolism
- From:Journal of Korean Medical Science
2013;28(10):1435-1442
- CountryRepublic of Korea
- Language:English
-
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.
