한빛사논문
- 조회1,820
Abstract
Yong-Geun Kwak1, Chang H. Song2, Ho K. Yi3, Pyoung H. Hwang3, Jong-Suk Kim4, Kyung S. Lee5 and Yong C. Lee5
1Department of Pharmacology, Institute of Cardiovascular Research, 2Department of Anatomy, 3Department of Pediatrics, 4Department of Biochemistry, and 5Department of Internal Medicine, Research Center for Allergic Immune Diseases, Chonbuk National University Medical School, Chonju, South Korea
Abstract
Phosphatase and tensin homologue deleted on chromosome ten (PTEN) is part of a complex signaling system that affects a variety of important cell functions. PTEN blocks the action of PI3K by dephosphorylating the signaling lipid phosphatidylinositol 3,4,5-triphosphate. We have used a mouse model for asthma to determine the effect of PI3K inhibitors and PTEN on allergen-induced bronchial inflammation and airway hyperresponsiveness. PI3K activity increased significantly after allergen challenge. PTEN protein expression and PTEN activity were decreased in OVA-induced asthma. Immunoreactive PTEN localized in epithelial layers around the bronchioles in control mice. However, this immunoreactive PTEN dramatically disappeared in allergen-induced asthmatic lungs. The increased IL-4, IL-5, and eosinophil cationic protein levels in bronchoalveolar lavage fluids after OVA inhalation were significantly reduced by the intratracheal administration of PI3K inhibitors or adenoviruses carrying PTEN cDNA (AdPTEN). Intratracheal administration of PI3K inhibitors or AdPTEN remarkably reduced bronchial inflammation and airway hyperresponsiveness. These findings indicate that PTEN may play a pivotal role in the pathogenesis of the asthma phenotype.
Address correspondence to: Yong Chul Lee, Department of Internal Medicine, Chonbuk National University Medical School, 634-18 Keumamdong, Chonju 561-712, South Korea. Phone: 82-63-250-1664; Fax: 82-63-254-1609
논문정보
- Research article
- 2003년 04월 (BRIC 등록일 )
- 국내 연구진
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