Abstract:

Abstract Objective To explore the possible molecular mechanism of epithelial-mesenchymal transition (EMT) and cell migration in high glucose (HG)-induced podocytes. Methodology: Immortalized conditional mouse podocytes (MPC5) worked as the research object. Podocytes were divided into HG group (stimulated with 30mmol/L glucose for 24 hrs), the normal glucose group (5 mmol/L glucose) and the mannitol group were set as control groups. Cell migration was examined by Transwell. The expression of protein was detected by Western blot. The mRNA level of protein was determined by qPCR. The nuclear translocation of NF-κB was observed by immunofluorescence. Results: Compared with the control groups, the cell migration was significantly enhanced (P<0.05), and the specific protein of podocytes’ Nephrin was significantly down-regulated (P<0.05). FN was significantly up-regulated (P<0.05) while E-cadherin was markedly down-regulated (P<0.05) after stimulated by HG for 24 hrs. Meanwhile, HG increased p-IκBα (P<0.05) and decreased IκBα (P<0.05) greatly, then promoted the nuclear translocation of NF-κB and up-regulated phosphorylation level of p65. Moreover, after treatment with the specific inhibitor Parthenolide (PTL), EMT and migration in podocytes were significantly inhibited and the protein level of Nephrin was up-regulated (P<0.05). Conclusions: HG induces EMT and cell migration in podocytes through NF-κB pathway.

Key words: high glucose, podocyte, epithelial-mesenchymal transition, cell migration, NF-κB