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Endothelin A Receptor (ETaR) siRNA Ameliorates Renal Ischemia Reperfusion Injury through Upregulating Expression of eNOS in Rats

Y. Jia, L. Li, T. Zhu.

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).

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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 May 11, 2025.

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