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(Pro)renin Receptor Regulates Phosphate Homeostasis in Rats via Releasing Fibroblast Growth Factor-23.
1Institute of Hypertension, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Frontiers in Physiology
|February 28, 2022
Summary
The (pro)renin receptor (PRR) plays a key role in phosphate regulation. PRR activation stimulates fibroblast growth factor 23 (FGF23) production, influencing phosphate excretion and metabolism.
Area of Science:
- Nephrology
- Endocrinology
- Mineral Metabolism
Background:
- Phosphate (Pi) homeostasis is crucial for life, with kidneys playing a central role.
- Fibroblast growth factor 23 (FGF23) from bone is a key endocrine regulator of Pi metabolism.
- The precise mechanisms linking Pi treatment to phosphaturic responses remain incompletely understood.
Purpose of the Study:
- To investigate the role of the (pro)renin receptor (PRR) in mediating the phosphaturic response to phosphate (Pi) administration.
- To elucidate the signaling pathway involving PRR, FGF23, and renal phosphate transporters.
Main Methods:
- Male Sprague-Dawley rats were pretreated with a PRR antagonist (PRO20) or vehicle.
- Rats received high phosphate (HP) solution, and Pi excretion was measured.
- FGF23, parathyroid hormone (PTH) levels, and renal Na/Pi-IIa expression were analyzed.
- Cultured osteoblast cells were used to study FGF23 expression in response to HP and PRR modulation.
Main Results:
- PRR antagonism with PRO20 significantly reduced HP-induced Pi excretion by 42%.
- PRO20 treatment blunted the upregulation of circulating FGF23 and PTH levels.
- Renal Na/Pi-IIa expression was downregulated in response to HP, an effect attenuated by PRO20.
- High Pi increased FGF23 expression in osteoblasts, which was inhibited by PRO20 or PRR siRNA.
Conclusions:
- The (pro)renin receptor (PRR) is a novel mediator of the phosphaturic response to phosphate loading.
- PRR activation stimulates FGF23 production, leading to increased Pi excretion.
- This pathway involves the subsequent downregulation of renal sodium-phosphate cotransporter Na/Pi-IIa.
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