IQGAP1 activates Tcf signal independent of Rac1 and Cdc42 in injury and repair of bronchial epithelial cells |
| |
Authors: | Wang Yongping Wang Aifeng Wang Fang Wang Mangxiang Zhu Min Ma Yan Wu Renliang |
| |
Affiliation: | a Institute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China b Key Laboratory of Pulmonary Disease of Ministry of Health of China, Wuhan 430030, PR China c Institute of Forensic Medicine, School of Basic Medical Sciences, Southern Medical University, 1838 North Guangzhou Street, Guangzhou 510515, PR China |
| |
Abstract: | The process of injury and repair involves spreading, migration and cell proliferation. The functions of Rho GTPases and their effector IQGAP1 are poor known in this process of airway epithelium. In the present study, we employed a widely used in vitro model by scratching a monolayer of BECs. We found that scratching induced decreasing of the GTP-bound Rac1 and Cdc42, but increasing the amounts of IQGAP1 at different time points. Next, we confirmed that IQGAP1 interacted with the constitutively active Rac1 (Rac1V12) and Cdc42 (Cdc42V12) rather than the dominant negative Rac1 (Rac1N17) and Cdc42 (Cdc42N17). Over-expressions of wild type (WT) IQGAP1 and its mutant (T1050AX2), which was defective to interact with Rho GTPases, induced translocation of β-catenin from the cytoplasm into the nucleus. These results activated Tcf/Lef and increased the expression levels of its target genes of c-myc and cyclin D1. Likewise, the amounts of c-myc and cyclin D1 increased after scratching. Our results suggested that IQGAP1 mediated cell proliferation through activating Tcf in a manner independent of Rac1 and Cdc42 in wound repair of BECs. |
| |
Keywords: | |
本文献已被 ScienceDirect PubMed 等数据库收录! |
|