Lina Yang1,2, Yi Fan2, Xiuli Zhang3, Lili Gao2, Jianfei Ma2. 1. Department of Geriatrics, The First Affiliated Hospital of China Medical University Shenyang 110001, Liaoning, P. R. China. 2. Department of Nephrology, The First Affiliated Hospital of China Medical University Shenyang 110001, Liaoning, P. R. China. 3. Department of Nephrology, Benxi Center Hospital, China Medical University Benxi 117000, Liaoning, P. R. China.
Abstract
OBJECTIVE: To explore the effects of miRNA-21/phosphatase and tensin homolog (PTEN) on the high glucose-stimulated epithelial-to-mesenchymal transition (EMT) in human peritoneal mesothelial cells (HPMCs). METHODS: HPMCs were cultured under control conditions, or with high glucose (HG), HG with miRNA-21 mimic or a miRNA-21 inhibitor. Expression of miRNA-21, α-smooth muscle actin, >fibronectin, E-cadherin and PTEN were measured by real time PCR, Western blotting and immunofluorescence staining. RESULTS: Compared with the control, HG induced the EMT, as shown by upregulation of α-smooth muscle actin and >fibronectin, and downregulation of E-cadherin. We also found that HG upregulated miRNA-21 expression and downregulated PTEN expression; the miRNA-21 inhibitor attenuated the HG-induced EMT in HPMCs by targeting PTEN; the miRNA-21 mimic increased the HG-induced EMT in HPMCs by targeting PTEN. CONCLUSIONS: This study demonstrated that miRNA-21 played a vital role in the HG-induced EMT by targeting PTEN in HPMCs.
OBJECTIVE: To explore the effects of miRNA-21/phosphatase and tensin homolog (PTEN) on the high glucose-stimulated epithelial-to-mesenchymal transition (EMT) in human peritoneal mesothelial cells (HPMCs). METHODS: HPMCs were cultured under control conditions, or with high glucose (HG), HG with miRNA-21 mimic or a miRNA-21 inhibitor. Expression of miRNA-21, α-smooth muscle actin, >fibronectin, E-cadherin and PTEN were measured by real time PCR, Western blotting and immunofluorescence staining. RESULTS: Compared with the control, HG induced the EMT, as shown by upregulation of α-smooth muscle actin and >fibronectin, and downregulation of E-cadherin. We also found that HG upregulated miRNA-21 expression and downregulated PTEN expression; the miRNA-21 inhibitor attenuated the HG-induced EMT in HPMCs by targeting PTEN; the miRNA-21 mimic increased the HG-induced EMT in HPMCs by targeting PTEN. CONCLUSIONS: This study demonstrated that miRNA-21 played a vital role in the HG-induced EMT by targeting PTEN in HPMCs.
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