LncRNA GAS5 reduces blood glucose levels and alleviates renal fibrosis in diabetic nephropathy by regulating the miR-542-3p/ERBB4 axis.

IF 3.4 3区医学 Q2 ENDOCRINOLOGY & METABOLISM

Diabetology & Metabolic Syndrome Pub Date : 2025-01-23 DOI:10.1186/s13098-025-01593-z

Qinghua Yin, Na Guo, Ruoxi Liao

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引用次数: 0

Abstract

Objective: The present study was implemented to unravel the effect of lncRNA GAS5 on renal fibrosis induced by diabetic nephropathy (DN) by regulating the miR-542-3p/ERBB4 axis.

Methods: db/db mice were injected with lncRNA GAS5 high expression or miR-542-3p low expression related vectors. Biochemical experiments were performed to assess blood glucose level and urine protein concentration. HE, TUNEL and Masson stainings were employed to observe the cellular morphology, apoptosis, and fibrosis of renal tissues, respectively. ELISA was executed to examine the levels of IL-1β, IL-6, and TNF-α; and the superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) activities were evaluated. Bioinformatics analysis, dual-luciferase and RIP assays were performed to verify the relationship between lncRNA GAS5 and miR-542-3p, and miR-542-3p and ERBB4.

Results: LncRNA GAS5 and ERBB4 were lowly expressed and miR-542-3p was highly expressed in the renal tissues of DN mice. Overexpression of lncRNA GAS5 or low-expression of miR-542-3p diminished DN-induced renal fibrosis. LncRNA GAS5 could bind to miR-542-3p and miR-542-3p further modulating ERBB4 expression. Up-regulation of miR-542-3p neutralized the suppressive effect of lncRNA GAS5 overexpression and down-regulation of ERBB4 also counteracted the inhibitory impact of down-regulation of miR-542-3p on renal fibrosis in DN mice.

Conclusion: Up-regulation of lncRNA GAS5 alleviates renal fibrosis in DN mice via down-regulation of miR-542-3p and up-regulation of ERBB4.

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来源期刊

Diabetology & Metabolic Syndrome ENDOCRINOLOGY & METABOLISM-

CiteScore

6.20

自引率

0.00%

发文量

170

审稿时长

7.5 months

期刊介绍： Diabetology & Metabolic Syndrome publishes articles on all aspects of the pathophysiology of diabetes and metabolic syndrome. By publishing original material exploring any area of laboratory, animal or clinical research into diabetes and metabolic syndrome, the journal offers a high-visibility forum for new insights and discussions into the issues of importance to the relevant community.