Endothelin A Receptor (ETaR) siRNA Ameliorates Renal Ischemia Reperfusion Injury through Upregulating Expression of eNOS in Rats
Shanghai Key Labratory of Organ Transplantation, Department of Urology, Zhongshan Hospital, Fudan University, Shanghai, China.
Meeting: 2018 American Transplant Congress
Abstract number: B29
Keywords: Endothelial cells, Endothelin, Ischemia, Kidney
Session Information
Session Name: Poster Session B: Endothelial Cell Biology
Session Type: Poster Session
Date: Sunday, June 3, 2018
Session Time: 6:00pm-7:00pm
Presentation Time: 6:00pm-7:00pm
Location: Hall 4EF
Aims: To explore the protective effect of Endothelin A Receptor (ETaR) siRNA on renal ischemia reperfusion injury and its underlying mechanism.
Methods: The model of unilateral ischemia reperfusion injury (IRI) in kidney of rats was established. Contralateral kidneys were removed
when reperfusion. Peripheral blood and kidney tissue samples were collected and examined 48h after surgery. Rats of drug group were treated with transfected ETaR siRNA vascular smooth muscle cells by renal intravenous hypertension perfusion of the kidneys during ischemia. The inhibitor group was treated with eNOS inhibitor L-NAME.
Results: The renal function and number of apoptotic cells were increased significantly. Renal tissue was injured seriously after renal
ischemia reperfusion in rats. PCR results showed that the expression of inflammatory factors and transcription factors caused by ischemia
reperfusion was reduced significantly after ETaR siRNA treatment. ELISA result showed that the level of eNOS in peripheral blood was decreased after renal ischemia reperfusion injury, while it was increased after the ETaR siRNA treatment. Western blot result displayed that ETaR siRNA treatment induced activation of PI3K/AKT and sGC/PKG signaling. While they were inhibited after L-NAME treatment.
Conclusion: ETaR siRNA is able to ameliorate renal function, reduce the amount of apoptotic cells, alleviate tissue injury. Its underlying
mechanisms may be that ETaR siRNA enhances eNOS activity through PI3K/AkT and decreases the expression of ET-1 by mediating
transcription factors activity via sGC/PKG signaling.
CITATION INFORMATION: Jia Y., Li L., Zhu T. Endothelin A Receptor (ETaR) siRNA Ameliorates Renal Ischemia Reperfusion Injury through Upregulating Expression of eNOS in Rats Am J Transplant. 2017;17 (suppl 3).
To cite this abstract in AMA style:
Jia Y, Li L, Zhu T. Endothelin A Receptor (ETaR) siRNA Ameliorates Renal Ischemia Reperfusion Injury through Upregulating Expression of eNOS in Rats [abstract]. https://atcmeetingabstracts.com/abstract/endothelin-a-receptor-etar-sirna-ameliorates-renal-ischemia-reperfusion-injury-through-upregulating-expression-of-enos-in-rats/. Accessed October 10, 2024.« Back to 2018 American Transplant Congress