Background: β-Catenin is a transcription factor to enhance the expression of several genes involved in cell proliferation and migration. Though it is clear that β-catenin plays an important role in neoplastic disease and during embryogenesis, little is known about its role in endothelial cell (EC). The aim of this study was to evaluate the β-catenin’s role in EC survival and function, and to identify a characteristic gene expression profile after adenoviral mediated β-catenin transfer. Methods: Human umbilical endothelial cells were infected with either wild type (WT) β-catenin or GFP using adenoviral vector (moi=50) in the 1% FBS. Under these conditions, transfection efficiency was 95% or greater. The pro-survival effect of β-catenin on EC was confirmed by WST-1 assay & FACS analysis. DNA chip analysis was used to describe candidate genes characteristic for β-catenin and these results were verified by RT-PCR and western blot. Results: Gene transfer of WT β-catenin protected EC from serum-deprivation-induced apoptosis in FACS analysis (sub-2N population of WT: GFP= 16.0: 42.3%, p<0.05) and induced EC proliferation in response to serum for 2days in WST-1 assay (WT: GFP= 204.9±15.6: 100.0±28.3%, p<0.05). Of ~10,000 genes examined by microarray, β-catenin signaling increased the expression of 64 genes and decreased 15 genes. Consistent with the pro-survival role of β-catenin, many transcription factor, growth factor, and cell cycle regulator genes were induced. β-catenin signaling also decreased the expression of several apoptotic gene. Among the candidate target genes of β-catenin, RT-PCR and western blot analysis showed significant increase of cyclin and heparan sulfate proteoglycan.Conclusion: These data show that β-catenin promotes the activation and survival of ECs. We were able to dissect β-catenin’s downstream target gene profile in ECs by DNA chip analysis, which showed that β-catenin turned on various genes for cell cycle progression and extra cellular matrix, and led to EC growth and survival.
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