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Updated: Apr 17, 2026
Detection of MicroRNA Expression in the Kidneys of Immunoglobulin A Nephropathic Mice
Published on: July 8, 2020
Reduced mir-29b-3p expression up-regulate CDK6 and contributes to IgA nephropathy
Li-Na Xing1, Hao Wang1, Pei-Hao Yin1
1Department of Nephrology, Putuo Hospital, Shanghai University of Traditional Chinese Medicine Shanghai 200062, China.
Abstract:
IgA nephropathy (IgAN) is the most common glomerulonephritis and the etiology of which is complex and multiple, and the pathological damage of IgAN is diversified. MicroRNA is a kind of gene expression suppressor and recently, researchers have found that microRNAs may play an important role in the pathogenesis of IgAN. Herein, we found that miR-29b-3p not miR-29a or miR-29c was significantly down regulated in IgAN patients' renal tissues. Predicted by bioinformatics tools and confirmed by dual luciferase assay and western blot, we found that the expression of CDK6 was repressed by miR-29b-3p directly. Subsequently, we found that miR-29b-3p down-regulation caused CDK6 overexpression can promote NF-κB signal by phosphorylating p65 which may enhance inflammation during IgAN pathogenesis.
Insights
MicroRNA-29b-3p is down-regulated in IgA nephropathy (IgAN), leading to increased CDK6. This promotes inflammation via the NF-κB pathway, contributing to kidney disease progression.
Area of Science:
- Nephrology
- Molecular Biology
- Genetics
Background:
- IgA nephropathy (IgAN) is a common kidney disease with complex causes and varied pathology.
- MicroRNAs are key regulators of gene expression and are implicated in IgAN pathogenesis.
Purpose of the Study:
- To investigate the role of miR-29b-3p in IgA nephropathy.
- To identify the downstream targets and signaling pathways affected by miR-29b-3p dysregulation in IgAN.
Main Methods:
- Analysis of miR-29b-3p expression in IgAN patient renal tissues.
- Bioinformatic prediction of miR-29b-3p targets.
- Dual luciferase assay and Western blot to confirm direct targeting of CDK6 by miR-29b-3p.
- Investigation of the effect of miR-29b-3p/CDK6 axis on the NF-κB signaling pathway.
Main Results:
- miR-29b-3p, but not miR-29a or miR-29c, was significantly downregulated in IgAN renal tissues.
- CDK6 was identified as a direct target gene repressed by miR-29b-3p.
- Downregulation of miR-29b-3p led to CDK6 overexpression, promoting NF-κB signaling by phosphorylating p65.
- This mechanism may contribute to inflammation in IgAN pathogenesis.
Conclusions:
- miR-29b-3p plays a protective role in IgA nephropathy by suppressing CDK6.
- The miR-29b-3p/CDK6/NF-κB axis represents a potential therapeutic target for mitigating inflammation in IgAN.
