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Updated: Nov 4, 2025
Nephrotoxin Microinjection in Zebrafish to Model Acute Kidney Injury
Published on: July 17, 2016
Reduced expression of MiR-125a-5p aggravates LPS-induced experimental acute kidney injury pathology by targeting
Chao Yang1, Cheng Yang1, Zhi Huang1
1Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, People's Republic of China.
Aims:
Patients with acute kidney injury (AKI) have higher mortality, and sepsis is among its main causes. MicroRNAs (miRNAs) are essential for regulating kidney function and could have curative potential. This study explored the possibility to treat AKI with miR-125a-5p and reveal the possible mechanism.
Materials And Methods:
LPS-induced mouse model and LPS-induced RAW264.7 cell model of AKI were established and treated with miR-125a-5p mimics or inhibitors. Serum creatinine and blood urea were measured to evaluate kidney function. The pathological changes of kidney tissues were detected by H&E and PAS staining technique, and the infiltration of macrophages were observed by immunohistochemistry. RAW264.7 cell viability, TRAF6 and cytokines expressions under LPS stimulation were measured. The role and therapeutic potential of miR-125a-5p were verified in vivo and in vitro after given miR-125a-5p mimics or inhibitors.
Key Findings:
LPS-induced mice had increasing serum creatinine and urea, and evident pathological changes, including severe tubular dilatation and macrophages infiltration. TRAF6 expression in the kidney was significantly higher, while miR-125a-5p expression was suppressed. MiR-125a-5p targeted TRAF6, and its overexpression deactivated NF-κB signaling pathway, reducing downstream TNF-α, IL-1β and IL-6 expressions. MiR-125a-5p mimics rescued LPS-induced kidney damage and suppressed pro-inflammatory cytokines expression through inhibiting TRAF6/NF-κB axis.
Significance:
We highlighted that miR-125a-5p could inhibit LPS-induced acute inflammation in the kidney through targeting TRAF6/NF-κB axis. These results might contribute to the development of molecular therapy in AKI.
Insights
MicroRNA-125a-5p (miR-125a-5p) shows potential in treating acute kidney injury (AKI) by targeting the TRAF6/NF-κB pathway. This molecular therapy may reduce inflammation and improve kidney function in sepsis-induced AKI.
Area of Science:
- Nephrology
- Molecular Biology
- Immunology
Background:
- Sepsis-induced acute kidney injury (AKI) is a critical condition with high mortality.
- MicroRNAs (miRNAs) play a crucial role in kidney function and hold therapeutic promise.
- Investigating specific miRNAs like miR-125a-5p is essential for understanding AKI pathogenesis.
Purpose of the Study:
- To explore the therapeutic potential of miR-125a-5p in treating lipopolysaccharide (LPS)-induced AKI.
- To elucidate the underlying molecular mechanism of miR-125a-5p in AKI.
Main Methods:
- Established LPS-induced mouse and RAW264.7 cell models of AKI.
- Administered miR-125a-5p mimics or inhibitors to assess therapeutic effects.
- Evaluated kidney function via serum creatinine and blood urea levels.
- Analyzed kidney tissue pathology, macrophage infiltration, and molecular signaling pathways (TRAF6, NF-κB, cytokines).
Main Results:
- LPS challenge led to impaired kidney function, pathological damage, and increased macrophage infiltration.
- miR-125a-5p expression was suppressed, while TRAF6 expression was elevated in LPS-induced AKI.
- miR-125a-5p directly targeted TRAF6, inhibiting the NF-κB signaling pathway.
- Overexpression of miR-125a-5p ameliorated kidney damage and reduced pro-inflammatory cytokine production.
Conclusions:
- miR-125a-5p effectively inhibits LPS-induced acute kidney inflammation by targeting the TRAF6/NF-κB axis.
- This miRNA represents a potential molecular therapeutic agent for AKI.
- Further research into miR-125a-5p could advance novel treatment strategies for AKI.
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