| First Author | Huang C | Year | 2016 |
| Journal | Biochem Biophys Res Commun | Volume | 478 |
| Issue | 1 | Pages | 181-186 |
| PubMed ID | 27453339 | Mgi Jnum | J:238862 |
| Mgi Id | MGI:5824450 | Doi | 10.1016/j.bbrc.2016.07.072 |
| Citation | Huang C, et al. (2016) Bevacizumab reduced auto-phosphorylation of VEGFR2 to protect HDM-induced asthma mice. Biochem Biophys Res Commun 478(1):181-6 |
| abstractText | Vascular endothelial growth factor (VEFG) is a major angiogenic factor involved in both normal physiological processes, such as embryonic development and wound healing, and in diseases, like cancer. Recent studies have revealed the functions of VEGF in inflammation and immunoregulation. Asthma is a chronic inflammation of the airways characterized by airway epithelial barrier dysfunction and imbalance in T-helper (Th) 1/Th2 during immunoregulation. We hypothesized that VEGF plays an important role in asthma. Utilizing a house dust mite extract (HDM)-induced murine model of asthma, we investigated whether bevacizumab, a humanized anti-VEGF monoclonal antibody, could protect the epithelial barrier in murine airways. We found that bevacizumab reduced airway hyper-responsiveness (AHR) and airway inflammation induced by HDM. In addition, HDM exposure promoted expression of VEGF, and caused AHR, disruptions of the epithelial barrier, and airway inflammation. Bevacizumab ameliorated AHR and the release of Th2 cytokines, thereby protecting the epithelial barrier. Our data suggest that bevacizumab may be a new therapeutic strategy for asthma. |
