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Updated: Apr 4, 2026
Bilateral Renal Ischemia-Reperfusion Model for Acute Kidney Injury in Mice
Published on: February 2, 2024
MRL/MpJ mice show unique pathological features after experimental kidney injury
Daichi Shiozuru1, Osamu Ichii1, Junpei Kimura1
1Laboratory of Anatomy, Department of Biomedical Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Hokkaido, Japan.
Abstract:
Clarification of the renal repair process is crucial for developing novel therapeutic strategies for kidney injury. MRL/MpJ mice have a unique repair process characterized by low scar formation. The pathological features of experimentally injured MRL/MpJ and C57BL/6 mouse kidneys were compared to examine the renal repair process. The dilation and atrophy of renal tubules were observed in folic acid (FA)-induced acute kidney injury (AKI) in both strains, and the histopathological injury scores and number of interleukin (IL)-1F6-positive damaged distal tubules and kidney injury molecule 1 (KIM-1)-positive damaged proximal tubules drastically increased 1 day after AKI induction. However, KIM-1-positive tubules and the elevation of serum renal function markers were significantly fewer and lower, respectively, in MRL/MpJ mice at days 2 and 7 after AKI. After traumatic kidney injury (TKI) via needle puncture, severe tubular necrotic lesions in the punctured area and fibrosis progressed in both strains. Indices for fibrosis such as aniline blue-positive area, number of alpha smooth muscle actin-positive myofibroblasts, and messenger RNA expression levels of Tgfb1 and Mmp2 indicated lower fibrotic activity in MRL/MpJ kidneys. Characteristically, only MRL/MpJ kidneys manifested remarkable calcification around the punctured area beginning 7 days after TKI. The pathological features of injured MRL/MpJ and C57BL/6 kidneys differed, especially those of kidneys with mild proximal tubular injuries after FA-induced AKI. Lower fibrotic activity and increased calcification after TKI were observed in MRL/MpJ kidneys. These findings clarified the unique pathological characteristics of MRL/MpJ mouse kidneys and contribute to understanding of the renal repair process after kidney injury.
Insights
MRL/MpJ mice exhibit unique kidney repair with less scarring and fibrosis compared to C57BL/6 mice after injury. These mice show distinct healing patterns, including increased calcification after traumatic injury.
Area of Science:
- Nephrology
- Regenerative Medicine
- Comparative Pathology
Background:
- Understanding kidney repair is vital for treating kidney injury.
- MRL/MpJ mice are known for reduced scar formation during tissue repair.
Purpose of the Study:
- To compare the renal repair processes in MRL/MpJ and C57BL/6 mice following kidney injury.
- To elucidate the unique pathological characteristics of MRL/MpJ kidneys in renal repair.
Main Methods:
- Induction of acute kidney injury (AKI) using folic acid (FA) in mice.
- Induction of traumatic kidney injury (TKI) via needle puncture.
- Histopathological analysis, including scoring of tubular damage and fibrosis.
- Assessment of specific markers like KIM-1, IL-1F6, alpha-smooth muscle actin, and calcification.
- Measurement of serum renal function markers and gene expression (Tgfb1, Mmp2).
Main Results:
- Both mouse strains showed tubular dilation and atrophy after FA-induced AKI.
- MRL/MpJ mice had significantly lower KIM-1 positive tubules and serum markers of renal dysfunction post-AKI.
- TKI led to tubular necrosis and fibrosis in both strains, but MRL/MpJ kidneys displayed reduced fibrotic activity.
- MRL/MpJ kidneys uniquely developed calcification around the injury site after TKI.
- Distinct pathological differences were observed, particularly in milder proximal tubular injuries.
Conclusions:
- MRL/MpJ mice demonstrate a unique renal repair profile characterized by lower fibrotic activity and increased calcification post-injury.
- These findings clarify the distinct pathological characteristics of MRL/MpJ kidneys and contribute to understanding renal repair mechanisms.
