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首页> 外文期刊>Journal of Cellular Physiology >Effect of adenosine triphosphate on phosphate uptake in renal proximal tubule cells: involvement of PKC and p38 MAPK.
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Effect of adenosine triphosphate on phosphate uptake in renal proximal tubule cells: involvement of PKC and p38 MAPK.

机译：三磷酸腺苷对磷酸盐的影响在肾近端小管细胞吸收:PKC和p38 MAPK的参与。

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摘要

ATP has been known to act as an extracellular signal and to be involved in various functions of kidney. Renal proximal tubular reabsorption of phosphate (Pi) contributes to the maintenance of phosphate homeostasis, which is regulated by Na+/Pi cotransporter. However, the effects of ATP on Na+/Pi cotransporters were not elucidated in proximal tubule cells (PTCs). Thus, the effects of ATP on Na+/Pi cotransporter and its related signal pathways are examined in the primary cultured renal PTCs. In the present study, ATP inhibited Pi uptake in a time (> 1 h) and dose (>10(-6)M) dependent manner. ATP-induced inhibition of Pi uptake was correlated with the decrease of type II Na+/Pi cotransporter mRNA. ATP-induced inhibition of Pi uptake may be mediated by P2Y receptor activation, since suramin (non-specific P2 receptor antagonist) and RB-2 (P2Y receptor antagonist) blocked it. ATP-induced inhibition of Pi uptake was blocked by neomycin, U73122 (phospholipase C (PLC) inhibitors), bisindolylmaleimide I, H-7, and staurosporine (protein kinase C (PKC) inhibitors), suggesting the role of PLC/PKC pathway. ATP also increased inositol phosphates (IPs) formation and induced PKC translocation from cytosolic fraction to membrane fraction. In addition, ATP-induced inhibition of Pi uptake was blocked by SB 203580 [a p38 mitogen activated protein kinase (MAPK) inhibitor], but not by PD 98059 (a p44/42 MAPK inhibitor). Indeed, ATP induced phosphorylation of p38 MAPK, which was not blocked by PKC inhibitor. In conclusion, ATP inhibited Pi uptake via PLC/PKC as well as p38 MAPK in renal PTCs.
机译：ATP一直作为细胞外信号和参与各种功能肾脏。磷酸(Pi)有助于维护磷酸体内平衡,这是规定Na + /π转运蛋白。在Na + /π转运蛋白没有阐明近端小管细胞(ptc)。ATP的Na + /π转运蛋白及其相关信号通路在初选中检查培养肾ptc(列车自动控制系统)。抑制π时间(> 1 h)和吸收剂量(> 10 (6) M)相关的方式。抑制π是与吸收降低II型Na + /π转运蛋白mRNA。ATP-induced抑制π吸收由P2Y受体激活,因为苏拉明(非特异性P2受体拮抗剂)RB-2 (P2Y受体拮抗剂)阻止了它。ATP-induced抑制π被吸收新霉素,U73122(磷脂酶C (PLC)抑制剂),bisindolylmaleimide我、第7和staurosporine(蛋白激酶C (PKC)抑制剂),表明PLC / PKC的角色途径。(IPs)形成和诱导PKC易位从胞质膜分数分数。此外,ATP-induced抑制π吸收被某人203580 (p38促分裂原激活蛋白激酶(MAPK)抑制剂),但不是通过PD98059 (p44/42 MAPK抑制剂)。p38 MAPK的磷酸化,不被PKC抑制剂。通过PLC / PKC抑制π吸收以及人们MAPK在肾ptc(列车自动控制系统)。

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