Abstract: SA-PO0262
Bicarbonate Ion Receptor GPR30 and Renal Ischemia-Reperfusion Injury
Session Information
- AKI: Mechanisms - Cell Signaling
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 103 AKI: Mechanisms
Authors
- Hirose, Hitomi, Department of Ion Signaling and Response, Sakaguchi Laboratory, Keio University School of Medicine, Shinjuku, Tokyo, Japan
- Gohda, Tomohito, Department of Nephrology, Juntendo University Faculty of Medicine, Bunkyo, Tokyo, Japan
- Suzuki, Yusuke, Department of Nephrology, Juntendo University Faculty of Medicine, Bunkyo, Tokyo, Japan
- Jo, Airi, Department of Ion Signaling and Response, Sakaguchi Laboratory, Keio University School of Medicine, Shinjuku, Tokyo, Japan
Background
Renal ischemia-reperfusion (I/R) injury causes acute kidney injury, contributes to renal dysfunction after kidney transplantation, and promotes the progression of chronic kidney disease. Renal I/R also induces marked alterations in pH and ion concentrations. GPR30 is a newly identified bicarbonate-sensing G protein-coupled receptor and elicits cellular responses in a pH-independent manner. This study aims to clarify the involvement of GPR30 in the pathophysiology of renal I/R injury.
Methods
Male C57BL/6 mice were used to establish a unilateral nephrectomy with contralateral renal (I/R) injury model. Mice were sacrificed at 24 hours or 7 days after I/R injury. Blood urea nitrogen (BUN) level was measured at 24 hours and/or 7 days after reperfusion. Histological analyses using Periodic acid-Schiff (PAS) staining was performed to evaluate proximal tubule injury. To analyze GPR30 expression, kidney tissue sections obtained from knock-in mice, in which the GPR30 coding sequence was replaced with the fluorescent protein Venus, were examined using confocal laser microscope. Renal blood flow during and after I/R injury was assessed using laser doppler flowmetry.
Results
BUN levels after renal I/R injury were lower in GPR30-deficient mice than those in control mice. Histological analysis showed prominent recovery of tubular injury in GPR30-deficient mice on day 7 after I/R injury. Venus expression, indicating the localization of GPR30, was observed in renal vessels and a part of renal tubules. Laser doppler flowmetry demonstrated dynamic changes in renal blood flow during and after I/R injury. In GPR30-deficient mice, no significant difference in renal blood flow was observed between baseline and 24 hours after I/R injury, whereas control mice showed a significant reduction in blood flow.
Conclusion
Compared with control mice, GPR30-deficient mice showed significant recovery from tubular injury and milder renal dysfunction following renal I/R injury. Reduced post-reperfusion blood flow mediated by arteriolar GPR30 may contribute to the progression of tubular injury. Our findings indicate that GPR30 is involved in the pathogenesis of renal I/R injury and may be a potential therapeutic target.