IQ domain GTPase-activating protein 1 mediates the process of injury and repair in bronchial epithelial cells.
- Author:
Yong-Ping WANG
1
;
Fang WANG
;
Man-Xiang WANG
;
Min ZHU
;
Yan MA
;
Ren-Liang WU
Author Information
1. Institute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Key Laboratory of Pulmonary Disease of Ministry of Health of China, Wuhan 430030, China.
- Publication Type:Journal Article
- MeSH:
Adenomatous Polyposis Coli Protein;
metabolism;
Animals;
Bronchi;
cytology;
Cell Proliferation;
Cells, Cultured;
Cytoskeleton;
metabolism;
Epithelial Cells;
cytology;
pathology;
Humans;
Mice;
Microtubule-Associated Proteins;
metabolism;
Neoplasm Proteins;
metabolism;
Nocodazole;
pharmacology;
Rats;
Swine;
Tubulin;
metabolism;
beta Catenin;
metabolism;
ras GTPase-Activating Proteins;
metabolism
- From:
Acta Physiologica Sinica
2008;60(3):409-418
- CountryChina
- Language:English
-
Abstract:
The process of injury and repair in airway epithelium involves cell spreading and migration followed by cell proliferation. IQ domain GTPase-activating protein 1 (IQGAP1) acts in a series of cell processes, but has not been clarified in lung epithelial cells. In this study, a widely used model of injury and repair in vitro by scratching bronchial epithelial cells (BECs) was utilized to investigate the function of IQGAP1. The results showed that IQGAP1 was abundant in BECs of mouse, rat, pig and human. IQGAP1 was colocalized with tubulin cytoskeleton, but was destroyed by nocodazole, a microtubule disassembly reagent. IQGAP1 mRNA and protein expressions increased at 6-9 h after scratching. In addition, overexpression of IQGAP1 translocated β-catenin from the cytoplasm into the nucleus and activated the Tcf/Lef signal. Scratching altered the associations of IQGAP1 with β-catenin, adenomatous polyposis coli (APC) and cytoplasmic linker protein-170 (CLIP-170). Silencing IQGAP1 expression by small interference RNA (siRNA) blocked the wound closure. It is concluded that IQGAP1 signal is involved in the wound closure of BECs induced by scratching.