Figure 2 of Ma, Mol Vis 2010; 16:2669-2679.


Figure 2. Immunocytochemistry was used to illustrate altered expression of VE-cadherin, β-catenin, vimentin, N-cadherin and protein kinase B (AKT2) in monkey choroid-retinal endothelial cells (RF/6A) and human umbilical vein endothelial cells (HUVEC) after the treatment by advanced glycation end products of BSA (AGE-BSA; 200 mg/l) for 24 h. For RF/6A cells, there were decreased expression of markers of endothelial cells, VE-cadherin (A) and β-catenin (B), and increased expression of markers of mesenchymal cells, N-cadherin (C) and vimentin (D). Similar to the RF/6A cells, the protein expression of VE-cadherin (F) and β-catenin (G) in the HUVEC cells was downregulated, and the expression of N-cadherin (H) and vimentin (I) in the HUVEC cells was upregulated. At the same time, the expression of Akt2 in the both cells increased (E, J). Additionally, in the RF/6A cells, the decreased part of β-catenin was mainly in the cytoplasm, while the protein expressed in the nucleus changed little (B); after treatment with AGE-BSA, N-cadherin expression was upregulated in the nucleus and downregulated in the intracytoplasm (D). In the HUVEC cells, there were no such phenomena.