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  • Title: Angiotensin-(1-7) attenuates high glucose-induced proximal tubular epithelial-to-mesenchymal transition via inhibiting ERK1/2 and p38 phosphorylation.
    Author: Zhou L, Xue H, Wang Z, Ni J, Yao T, Huang Y, Yu C, Lu L.
    Journal: Life Sci; 2012 Mar 10; 90(11-12):454-62. PubMed ID: 22285598.
    Abstract:
    AIMS: The kidney is an important target for both Angiotensin II and angiotensin-(1-7) [Ang-(1-7)] in the renin-angiotensin system. However, the renal function of Ang-(1-7) remains unclear. This study is aimed at investigating the effect of Ang-(1-7) on high glucose-induced epithelial to mesenchymal transition (EMT) in cultured renal epithelial cells. MAIN METHODS: Cultured renal epithelial (NRK-52E) cell line was used in the experiment. Fluorescence immunocytochemistry was performed to observe α-smooth muscle actin (α-SMA). Real-time PCR and Western blot were used to determine mRNA and protein levels. Enzyme-linked immunosorbent assay was used to measure the concentration of transforming growth factor-β1 (TGF-β1) in the culture media. KEY FINDINGS: High glucose-induced decreased in both angiotensin-converting enzyme-related carboxypeptidase (ACE2) and Mas mRNA levels. Meanwhile, high glucose induced increases in α-SMA and vimentin, decreases in E-cadherin, elevations in TGF-β1 and fibronectin secretions. Ang-(1-7) partially reversed high glucose-induced changes in α-SMA, vimentin, E-cadherin, TGF-β1 and fibronectin. High glucose stimulated ERK, p38 and JNK phosphorylation and Ang-(1-7) reversed the changes in ERK and p38 but not JNK phosphorylation. SIGNIFICANCE: Inhibition and insufficiency in ACE2-Ang-(1-7)-Mas axis under high glucose condition participate EMT. Supplementation of Ang-(1-7) attenuates high glucose-induced EMT. ERK and p38 intracellular signaling pathways, not JNK, mediate the effect of Ang-(1-7) on EMT.
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