Abstract

Key Laboratory of Transplant Engineering and Immunology. Background Acute kidney injury (AKI) is a serious worldwide health issue with high mortality and morbidity. Kidney is a high energy-demanding organ that requires well-functioning mitochondria. MSCs have shown multiple benefits to AKI, but their specific role on renal mitochondria is not clear. In this study, we evaluated the effects of MSCs on renal function and mitochondrial injury in AKI mice. Methods: MSCs isolated from C57/BL6 mice were infused into ischemic-reperfusion (I/R)-induced AKI mice via tail vein injection. Mice were sacrificed at 5 days after surgery, and blood/kidney samples were collected for clinical biochemistry, real-time PCR, TEM and histological examination. Results: MSCs significantly improved renal function with decreased levels of serum BUN/CREA and renal necrotic tubules, and reduced KIM-1 (renal injury marker) and inflammatory cytokines (IL-1β/ICAM-1) in AKI mice. Moreover, BMSCs significantly rescued renal mitochondrial lesions with reduced mtROS, increased levels of ATP, mtDNA copy number, TFAM (master mediator of mtNDA transcription), mitochondrial biogenesis-related genes (PGC1-α, ATP5a-1, NDUFS8), and elevated mitochondrial cristae density and length/width ratio in AKI mice. Conclusion: This study indicated that MSCs therapy could ameliorate renal dysfunction after AKI, and their renal protective effects were through enhancing mtDNA transcription and mitochondrial biogenesis. This work was supported by grants from National Natural Science Foundation of China (31200754, 81571808, 31871001)..

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