Role for integrin-linked kinase in mediating tubular epithelial to mesenchymal transition and renal interstitial fibrogenesis
J. Clin. Invest. Yingjian Li, et al. 112:503 doi:10.1172/JCI17913 [Go to this article.]

Figure 3
Forced expression of ILK suppresses E-cadherin expression in tubular epithelial cells in a dose-dependent manner. Stable cell lines were established by transfection of WT-ILK and kd-ILK expression vectors. A cell line with mock transfection of empty vector pUSEamp plasmid (Vector) was used as control. (a) Cell lysates were immunoblotted with Ab’s against ILK, E-cadherin, and actin, respectively. Numbers (C1, C2, and C3) indicate three individual clones that express different levels of ILK. (b) Linear regression shows a close association between ILK and E-cadherin in tubular epithelial cells. The correlation coefficients (R²) are shown. The relative abundances of ILK and E-cadherin were normalized to actin. (c–f) Immunofluorescence staining shows an inverse relationship between ILK and E-cadherin expression in HKC cells transfected with empty vector (c and e) or WT-ILK (d and f). (c and d) ILK staining. (e and f) E-cadherin staining. Scale bars, 5 μm. (g and h) Suppression of E-cadherin expression by ILK is independent of Snail. Neither TGF-β1 (g) nor ILK (h) induced Snail expression in tubular epithelial cells. HKC cells were treated with 2 ng/ml of TGF-β1 for various periods of time as indicated (g), or transfected (either transiently or stably) with WT-ILK and kd-ILK expression vectors (h). HKC cells transiently transfected with Snail expression vector served as positive control for Snail protein expression.