Insulin-like growth factor binding protein-5 enhances the migration and differentiation of gingival epithelial cells

被引:11
作者
Hung, P. -S. [1 ]
Kao, S. -Y. [2 ]
Liu, C. -J. [1 ,3 ]
Tu, H. -F. [1 ,2 ]
Wu, C. -H. [1 ,2 ]
Lin, S. -C. [1 ]
机构
[1] Natl Yang Ming Univ, Sch Dent, Inst Oral Biol, Taipei 112, Taiwan
[2] Taipei Vet Gen Hosp, Dept Dent, Taipei, Taiwan
[3] Taipei Mackay Mem Hosp, Dept Dent, Taipei, Taiwan
关键词
differentiation; gingiva; insulin-like growth factor binding protein-5; involucrin; keratinocyte; transglutaminase-1;
D O I
10.1111/j.1600-0765.2007.01070.x
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
The objective was to define the roles of insulin-like growth factor binding protein-5 (IGFBP-5) in gingival epithelial cells (GEC). Human IGFBP-5 is expressed in many cell types and has diverse biological functions. It stimulates the growth of bone cells and is associated with the impedance of gingival fibroblast apoptosis. In gingival epithelium, IGFBP-5 is expressed in the cells of the differentiated stratum spinosum layer. Recombinant IGFBP-5 protein treatment and knockdown of IGFBP-5 expression using a lentivirus-delivered short hairpin RNA was carried out in human GEC. Proliferation, apoptosis, anoikis, migration, differentiation and gene expression in GEC were analyzed and molecular images were obtained. The IGFBP-5 had no effect on proliferation, but it slightly suppressed apoptosis and anoikis of GEC. It also induced GEC migration and upregulated the expression of involucrin, transglutaminase-1, keratin and focal adhesion kinase. The IGFBP-5 induced migration partly via an insulin-like growth factor-independent mechanism. The knockdown of IGFBP-5 downregulated the expression of involucrin, transglutaminase-1 and focal adhesion kinase. Expression of IGFBP-5 in GEC is associated with anti-apoptosis, migration and differentiation of GEC. These phenotypic effects may be associated with focal adhesion kinase and are advantageous for re-epithelization of GEC and the maintenance of gingival health.
引用
收藏
页码:673 / 680
页数:8
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