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Updated: Jan 16, 2026

A Quantitative Detection Method for MicroRNAs in the Kidney of an Ischemic Kidney Injury Mouse Model
Published on: September 11, 2020
Sepsis-associated acute kidney injury in mice and humans elicits heterogeneous renal microvascular microRNA responses
Matthijs Luxen1,2, Tamar J van der Aart3, Rianne M Jongman1,4
1Department of Pathology and Medical Biology, Medical Biology section, University Medical Center Groningen, University of Groningen, 5617 Hanzeplein 1, Groningen, 9713 GZ, the Netherlands.
Abstract:
Microvascular endothelial cells play important roles in sepsis-associated acute kidney injury (SA-AKI). In this study, we focused on microvascular microRNAs changes following SA-AKI to identify microRNAs as novel druggable targets and microvasculature-related early biomarkers of SA-AKI. Using small RNA sequencing we identified 40 differentially expressed microRNAs in the renal microvasculature in response to SA-AKI. While the induction of most microRNAs was restricted to a single microvascular compartment, miR-21-5p levels were increased across the renal microvasculature in both mice and humans following SA-AKI. Functional assessment in vitro revealed that inhibition of hsa-miR-21-5p exacerbated endothelial inflammatory activation, suggesting a protective role of this microRNA in endothelial cells. Furthermore, patients with SA-AKI exhibited elevated hsa-miR-21-5p levels in plasma compared with critically ill sepsis patients without AKI. These results highlight the potential of hsa-miR-21-5p and other microRNAs as therapeutic targets and biomarkers in SA-AKI.
Insights
MicroRNAs, including miR-21-5p, are altered in sepsis-associated acute kidney injury (SA-AKI). Elevated miR-21-5p in plasma may serve as an early biomarker and potential therapeutic target for SA-AKI.
Area of Science:
- Renal physiology and pathology
- Molecular biology
- Biomarker discovery
Background:
- Sepsis-associated acute kidney injury (SA-AKI) involves microvascular endothelial cells.
- MicroRNAs (miRNAs) are crucial regulators of cellular processes and are implicated in disease.
- Identifying novel biomarkers and therapeutic targets for SA-AKI is critical.
Purpose of the Study:
- To investigate changes in microvascular miRNAs in SA-AKI.
- To identify potential druggable miRNA targets and early biomarkers for SA-AKI.
- To elucidate the role of specific miRNAs, such as miR-21-5p, in SA-AKI pathogenesis.
Main Methods:
- Small RNA sequencing was employed to profile miRNA expression in the renal microvasculature of SA-AKI models.
- In vitro functional assays were conducted to assess the role of hsa-miR-21-5p in endothelial cells.
- Plasma hsa-miR-21-5p levels were measured in patients with SA-AKI and sepsis without AKI.
Main Results:
- Forty differentially expressed miRNAs were identified in the renal microvasculature during SA-AKI.
- miR-21-5p levels were significantly increased across the renal microvasculature in both mice and humans with SA-AKI.
- Inhibition of hsa-miR-21-5p worsened endothelial inflammatory activation, indicating a protective role.
- Elevated plasma hsa-miR-21-5p levels were observed in SA-AKI patients compared to sepsis patients without AKI.
Conclusions:
- Microvascular miRNA dysregulation is a feature of SA-AKI.
- hsa-miR-21-5p demonstrates a protective role in endothelial cells during SA-AKI.
- hsa-miR-21-5p is a promising candidate for an early plasma biomarker and a potential therapeutic target for SA-AKI.
Related Concept Videos
Acute Kidney Injury II: Pathophysiology
Acute Kidney Injury I: Introduction
Acute Kidney Injury IV: Diagnostic Studies and Prevention
Acute Kidney Injury III: Clinical Manifestations

