Ang-(1–7) inhibited mitochondrial fission in high-glucose-induced podocytes by upregulation of miR-30a and downregulation of Drp1 and p53

Abstract

BackgroundThe aim of this study was to investigate the possible effects of angiotensin-(1–7) [Ang-(1–7)] on podocytes and the mitochondrial signaling pathway in a high-glucose (HG) environment. MethodsWe established a model of HG-induced podocytes by incubating podocytes in RPMI 1640 containing 33mM glucose. The cells were divided into the following groups: (1) normal glucose group as control incubated in Roswell Park Memorial Institute (RPMI) 1640 containing 5mM glucose; (2) Ang-(1–7), 10nM, incubated in RPMI 1640 containing 5mM glucose; (3) the HG group incubated in RPMI 1640 containing 33mM glucose; and (4) Ang-(1–7), 10nM, incubated in HG group incubated in RPMI 1640 containing 33mM glucose. After a period of 24 hours, mitochondrial fission and podocyte fusion were observed by electron microscope. Additionally, p53 and Drp1 were tested by Western blot, the position of Drp1 was detected by immunofluorescence, and miR-30a was analyzed by quantitative real-time polymerase chain reaction. ResultsAng-(1–7) inhibited mitochondrial fission in HG-treated podocytes. However, Ang-(1–7) also significantly reduced the expression of Drp1 and p53, and improved the expression of miR-30a in HG-induced podocytes. ConclusionAng-(1–7) inhibited mitochondrial fission in HG-induced podocytes by upregulation of miR-30a and downregulation of Drp1 and p53.