Downregulation of renal type IIa sodium-dependent phosphate cotransporter during lipopolysaccharide-induced acute inflammation

被引:13
|
作者
Ikeda, Shoko [1 ]
Yamamoto, Hironori [3 ,4 ]
Masuda, Masashi [1 ]
Takei, Yuichiro [1 ]
Nakahashi, Otoki [1 ]
Kozai, Mina [1 ]
Tanaka, Sarasa [1 ]
Nakao, Mari [1 ]
Taketani, Yutaka [1 ]
Segawa, Hiroko [2 ]
Iwano, Masayuki
Miyamoto, Ken-ichi [2 ,4 ]
Takeda, Eiji [1 ]
机构
[1] Univ Tokushima, Inst Hlth Biosci, Dept Clin Nutr, Kuramoto, Tokushima, Japan
[2] Univ Tokushima, Inst Hlth Biosci, Dept Mol Nutr, Kuramoto, Tokushima, Japan
[3] Jin Ai Univ, Fac Human Life, Dept Hlth & Nutr, Echizen City, Fukui 9158586, Japan
[4] Univ Fukui, Fac Med Sci, Dept Gen Med, Div Nephrol, Fukui 910, Japan
关键词
LPS; phosphate; kidney; Npt2a; PTH; FGF23; GENE-EXPRESSION; PARATHYROID-HORMONE; VITAMIN-D; 1,25-DIHYDROXYVITAMIN D-3; TRANSCRIPTIONAL CONTROL; DIETARY PHOSPHATE; TRANSPORTERS; SEPSIS; BONE; NPT2A;
D O I
10.1152/ajprenal.00474.2013
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The type IIa sodium-dependent phosphate cotransporter (Npt2a) plays a critical role in reabsorption of inorganic phosphate (P-i) by renal proximal tubular cells. P-i abnormalities during early stages of sepsis have been reported, but the mechanisms regulating P-i homeostasis during acute inflammation are poorly understood. We examined the regulation of P-i metabolism and renal Npt2a expression during lipopolysaccharide (LPS)-induced inflammation in mice. Dose-response and time-course studies with LPS showed significant increases of plasma P-i and intact parathyroid hormone (iPTH) levels and renal P-i excretion, while renal calcium excretion was significantly decreased. There was no difference in plasma 1,25-dihydroxyvitamin D levels, but the induction of plasma intact fibroblast growth factor 23 levels peaked 3 h after LPS treatment. Western blotting, immunostaining, and quantitative real-time PCR showed that LPS administration significantly decreased Npt2a protein expression in the brush border membrane (BBM) 3 h after injection, but there was no change in renal Npt2a mRNA levels. Moreover, tumor necrosis factor-alpha injection also increased plasma iPTH and decreased renal BBM Npt2a expression. Importantly, we revealed that parathyroidectomized rats had impaired renal P-i excretion and BBM Npt2a expression in response to LPS. These results suggest that the downregulation of Npt2a expression in renal BBM through induction of plasma iPTH levels alter P-i homeostasis during LPS-induced acute inflammation.
引用
收藏
页码:F744 / F750
页数:7
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