Abstract
Background: In order to investigate the mechanism through which Early growth response protein 1 (Egr1) mediates long noncoding RNA Arid2-IR to promote diabetic kidney disease. Method: In vivo, we induced type 2 diabetes and overexpressed or knocked down Egr1 by rapidly injecting of a large volume of DNA solution through the tail vein. In vitro, we assessed mouse mesangial cells that were stimulated with high glucose conditions and transiently transfected with siRNA and plasmids. Results: Compared with those in the control group, the expression of Egr1 and Arid2-IR in diabetes mice increased with the up-regulation of Col1a1 and α-SMA. Arid2-IR expression changes with Egr1 knockdown and overexpression both in vivo and in vitro. Knockdown Arid2-IR in vitro reduced Col1a1 and α-SMA expression. Overexpressing Egr1 and silencing Arid2-IR reduced Col1a1 and α-SMA expression. Conclusion: Egr1 promoted ECM production by up-regulating Arid2-IR. Thus, Arid2-IR may be a new target for treating diabetic kidney disease. Disclosure Y. Yang: None. F. Hu: None. M. Xue: None. Y. Jia: None. M. Zou: None. Y. Xue: None.
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