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Updated: Nov 16, 2025
A Quantitative Detection Method for MicroRNAs in the Kidney of an Ischemic Kidney Injury Mouse Model
Published on: September 11, 2020
Long Non-Coding RNA RMRP Contributes to Sepsis-Induced Acute Kidney Injury
Xia Zhang1, Zhongwei Huang2, Yan Wang1
1Department of Emergency, Affiliated Hospital of Nantong University, Nantong, China.
Purpose:
This study aimed to explore the role of the long non-coding RNA (lncRNA) RNA component of mitochondrial RNAase P (RMRP) in sepsis-induced acute kidney injury (AKI).
Materials And Methods:
Venous blood was collected from septic patients and healthy people. C57BL/6 mice who underwent cecal ligation and puncture (CLP) were used as in vivo models of septic AKI. Lipopolysaccharide (LPS)-induced HK-2 cells were employed as in vitro models of AKI. Flow cytometry analysis was conducted to detect cell apoptosis. Enzyme-linked immunosorbent assay and Western blot assays were used to detect levels of pro-inflammatory cytokines.
Results:
RMRP was upregulated in sera from patients with AKI and in LPS-induced cells. Knockdown of RMRP inhibited cell apoptosis and reduced production of inflammatory factors in LPS-induced cells, as well as alleviated AKI in CLP mice. RMRP facilitated inflammation by activating NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome. We found that microRNA 206 (miR-206) binds with and is negatively regulated by RMRP: miR-206 directly targets the 3' untranslated region of DEAD-box helicase 5 (DDX5) and negatively regulates DDX5 expression. By binding with miR-206, RMRP upregulated DDX5 expression. Rescue assays revealed that overexpression of DDX5 counteracted the effect of RMRP inhibition on cell apoptosis and inflammatory response in LPS-induced cells.
Conclusion:
The lncRNA RMRP contributes to sepsis-induced AKI through upregulation of DDX5 in a miR-206 dependent manner and through activation of NLRP3 inflammasome. This novel discovery may provide a potential strategy for treating AKI.
Insights
The long non-coding RNA RMRP exacerbates sepsis-induced acute kidney injury by activating the NLRP3 inflammasome and upregulating DDX5 via miR-206. Inhibiting RMRP shows therapeutic potential for sepsis-related AKI.
Area of Science:
- Molecular Biology
- Immunology
- Renal Physiology
Background:
- Sepsis-induced acute kidney injury (AKI) is a critical complication with high mortality.
- The role of long non-coding RNAs (lncRNAs) in sepsis-AKI pathogenesis remains incompletely understood.
Purpose of the Study:
- To investigate the function of the lncRNA RNA component of mitochondrial RNAase P (RMRP) in sepsis-induced AKI.
- To elucidate the molecular mechanisms underlying RMRP's involvement in AKI.
Main Methods:
- Analysis of RMRP expression in patient sera and cell/animal models of AKI.
- In vitro and in vivo experiments involving RMRP knockdown and overexpression.
- Assessment of inflammatory cytokines, cell apoptosis, and inflammasome activation (NLRP3).
- Investigation of the RMRP-miR-206-DDX5 regulatory axis.
Main Results:
- RMRP expression was significantly upregulated in sepsis-AKI patients and models.
- RMRP knockdown ameliorated AKI, reduced apoptosis, and suppressed pro-inflammatory cytokine production.
- RMRP promoted inflammation by activating the NLRP3 inflammasome.
- RMRP upregulated DEAD-box helicase 5 (DDX5) expression by sponging microRNA 206 (miR-206).
- Overexpression of DDX5 reversed the protective effects of RMRP inhibition.
Conclusions:
- The lncRNA RMRP plays a crucial role in sepsis-induced AKI.
- RMRP contributes to AKI by activating the NLRP3 inflammasome and upregulating DDX5 in a miR-206-dependent manner.
- Targeting RMRP presents a potential therapeutic strategy for sepsis-AKI.
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