Cabin1 is upregulated during podocyte mitochondrial dysfunction induced by Angiotensin Ⅱ

CHEN Jieru; LI Huiyuan; WEN Yueqiang

doi:10.3969/j.issn.1006-5725.2017.23.004

Abstract：Objective To investigate the role of Calcineurin binding protein 1(Cabin1)in podocyte mito-chondrial dysfunction. Methods Cultured podocytes were injured by AngiotensinⅡ(AngⅡ).Cells were harvest-ed after 0 h,24 h and 48 h after AngⅡstimulating.Immunofluorescence staining was used to observe the disrup-tion of actin cytoskeleton,as well as the distribution of Cabin1.Western bolt was applied to detect the level of cyto-chrome c and Cabin1 protein in podocytes. Results AngⅡremarkably caused podocyte damage in a time depen-dent manner. Phalloidin staining displayed strong and long bundles of intracellular actin filaments in untreated cells. AngⅡ induced the loss of the cytoplasmic cytoskeleton and the reorganized of actin cytoskeleton at 24 and 48h. In normal podocytes,Cabin1 evenly localized in the cytoplasm and nuclei. AngⅡinduced strong staining of Cabin1 in podocytes nuclei. Cytochrome c and Cabin1 protein expression apparently increased in AngⅡ injuried podocyte.Ctyochrome c protein obviously increased in cells at 24 h and 48 h after AngⅡstimulating,which were as 1.51 and 1.87 times as the normal control group(P < 0.05). Similarly,the expression of Cabin1 were as 1.33 and 1.67 times respectively in 24 h and 48 h while compared to the normal control group(P < 0.05). Conclu-sion Cabin1 was overexpressed during podocyte mitochondrial dysfunction.It could be a crucial factor which regu-lates mitochondrial function during podocyte damage.