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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Meng, Qiu Fang, Cailong Wang, Wei Wang, Yui-hsi Lv, Ze Lee, Tak H. Wu, Huifen Corrigan, Chris J. Reay, Victoria Fan, Yiqiang Liu, Yong-jun Ying, Sun An, Yunqing |
| Description | Author Affiliation: Corrigan CJ ( Division of Asthma, Allergy and Lung Biology, King's College London, Medical Research Council, and Asthma UK Centre in Allergic Mechanisms of Asthma, London SE1 9RT, United Kingdom.); |
| Abstract | IL-25 (IL-17E) is a T-helper cell type 2 (Th2) cytokine best described as a potentiator of Th2 memory responses. Reports of expression of its receptor, IL-25R, on airways structural cells suggest a wider role for IL-25 in remodeling. We hypothesized that IL-25 stimulates local angiogenesis in the asthmatic bronchial mucosa. Immunoreactive IL-25(+), IL-25R(+), and CD31(+) (endothelial) cells in sections of bronchial biopsies from asthmatics and controls were detected by immunohistochemistry. The effect of IL-25 on angiogenesis was examined using an in vitro assay. Real-time PCR was used to detect expression of IL-25R and VEGF mRNA in cultured human vascular endothelial cells (HUVEC), and a cell proliferation kit (WST-8) was used to measure the effect of IL-25 on HUVEC proliferation. Immunostaining showed that IL-25(+), IL-25R(+), and CD31(+)/IL-25R(+) cells were significantly elevated in the bronchial mucosa of asthmatics compared with controls (P < 0.003). In asthmatics, the numbers of IL-25(+) cells correlated inversely with the forced expiratory volume in 1 s (r = -0.639; P = 0.01). In vitro, HUVEC constitutively expressed IL-25R, which was up-regulated further by TNF- . IL-25 and TNF- also increased expression of VEGF and VEGF receptors. IL-25 increased HUVEC proliferation and the number, length, and area of microvessel structures in a concentration-dependent manner in vitro. VEGF blockade, the PI3K-specific inhibitor LY294002, and the MAPK/ERK1/2 (MEK1/2)-specific inhibitor U0126 all markedly attenuated IL-25-induced angiogenesis, and the inhibitors also reduced IL-25-induced proliferation and VEGF expression. Our findings suggest that IL-25 is elevated in asthma and contributes to angiogenesis, at least partly by increasing endothelial cell VEGF/VEGF receptor expression through PI3K/Akt and Erk/MAPK pathways. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 4 |
| Volume Number | 108 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2011-01-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Asthma Immunology Bronchi Blood Supply Interleukin-17 Th2 Cells Antigens, CD31 Genetics Metabolism Physiopathology Blotting, Western Drug Effects Pathology Cell Proliferation Cells, Cultured Endothelial Cells Extracellular Signal-Regulated MAP Kinases Immunohistochemistry Immunologic Memory Pharmacology Phosphatidylinositol 3-Kinases Phosphorylation Proto-Oncogene Proteins C-akt Receptors, Interleukin Reverse Transcriptase Polymerase Chain Reaction STAT6 Transcription Factor Vascular Endothelial Growth Factor A Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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