Abstract: PO2615
Renal Denervation Alleviates Renal Ischemic-Reperfusion Injury-Induced Acute and Chronic Kidney Injury Partly by Modulating MiRNAs in Rats
Session Information
- AKI Epidemiology, Risk Factors, and Prevention: Basic Science
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 101 AKI: Epidemiology, Risk Factors, and Prevention
Author
- Zou, Xiangyu, Shanghai Childrens Medical Center Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China
Background
Renal denervation (RDN) has been used as a potential medium for kidney injury repair and miRNAs involved in the pathophysiology of renal injury. However, the change of miRNAs after RDN and its proper protective mechanisms has yet to be determined.
Methods
Renal ischemic reperfusion injury (IRI) rat model was established and RDN was applied. Animals were sacrificed at 24 hours and 2 weeks after operation. Tyrosine hydroxylase (TH), renal functions, tubular cell apoptosis and histology staining were examined at 24 hours, and renal fibrosis and capillary vessels were measured at 2 weeks. What is more, the expression of miRNAs in injured kidney was determined by micro-array and the target genes were analyzed. Lastly, human renal biopsy samples with chronic kidney disease were picked for the TH and fibrosis analysis.
Results
TH was eliminated and renal functions were improved in the denervation group at 24 hours. RDN reduce tubular cell apoptosis and mitigate the histological lesion. Meanwhile, the increase of capillary vessel density and reduce of renal fibrosis was observed after 2 weeks. Moreover, numbers of miRNAs were up-regulated after RDN treatment both at 24 hours and 2 weeks, and the miRNA targeted pro-angiogenesis, anti-fibrosis and inflammatory pathways were modulated. Lastly, less fibrosis regions were found in TH high expression regions of human renal biopsy samples.
Conclusion
RDN was a reliable method in alleviating IRI induced acute and chronic kidney injury, and the modulation of miRNA related pro-angiogenesis, anti-fibrosis or inflammatory pathways involved in this process.