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Gene expression changes induced by over-expression of miR-181b-5p in db/db mouse

ABSTRACT: The microRNAs (miRNAs) that can influence diabetic kidney disease (DKD) have not been fully characterized. The aim of this study was to identify the miRNAs that affect DKD and could be used as specific biomarkers or therapeutic agents. First, kidneys from two DKD mouse models were screened for differences in miRNA expression from control mice. We found that miRNA-125b-5p and miRNA-181-5p were specifically differentially expressed in the kidneys of DKD mice. Next, we administered miRNA-181b-5p-mimic to DKD mice, which reduced the albuminuria and abnormal mesangial expansion. Pathway analysis revealed that overexpression of miRNA-181-5p significantly altered the expression of 51 genes in the kidneys of DKD mice. Furthermore, the serum level of miRNA-125b-5p was significantly higher and that of miRNA-181-5p was lower in patients with DKD than in patients with other kidney diseases. These results suggest that miRNA-125b-5p and miRNA-181b-5p may represent novel diagnostic biomarkers and that miRNA-181b-5p may represent a therapeutic target for DKD.

ORGANISM(S): Mus musculus

PROVIDER: GSE161885 | GEO | 2020/12/21

REPOSITORIES: GEO

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Project description:Purpose: Our study clarifies the mechanism of Huangqi decoction (HQD) against DKD in diabetic db/db mice. Methods: Eight-week-old male diabetic db/db mice were randomly divided into four groups: Model (1% CMC), HQD-L (0.12 g/kg), HQD-M (0.36 g/kg), and HQD-H (1.08 g/kg) groups. Non-diabetic db/m mice were used as a control group. These mice received HQD treatment for 8 weeks continuously. After 8 weeks of feeding, kidneys were harvested to observe the kidney function, pathological changes, micro-assay study, and the protein expression levels. Results: HQD treatment improved the albumin/creatine ratio (ACR) and 24 h urinary albumin, prevented the pathological phenotypes of increased glomerular volume, widened mesangial areas, the proliferation of mesangial matrix, the disappearance of foot processes, the decreased expression of nephrin and the number of podocytes. The expression profile chips were assessed to reveal the global transcriptional response and predict related functions, diseases and pathways. To verify this, we found that HQD treatment activated the protein expressions of BMP1, BMP7, BMPR2, and active-Rap1 and inhibited Smad1 and phospho-ERK. In addition, HQD could improve lipid deposition in the kidneys of db/db mice. Conclusion: HQD prevents the progression of DKD in db/db mice by regulating the transcription of BMPs and their downstream target genes, inhibiting the phosphorylation of ERK and Smad1 by promoting the binding of Rap1 to GTP and regulating the lipid metabolism dysfunction. These provide a new idea for the treatment of DKD. Overall, HQD had a significant protective effect against DKD. This may be related to the fact that HQD promotes the transcription of BMPs and their downstream target genes by upregulating BMPR-II and regulates the phosphorylation of ERK and Smad by promoting the binding of Rap1 to GTP. In addition, HQD also has a noticeable role in regulating lipid metabolism dysfunction in DKD, which provides a new idea for future research on HQD.

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Gene expression changes induced by over-expression of miR-181b-5p in db/db mouse

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