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Estradiol-17beta stimulates phosphate uptake and is mitogenic for primary rabbit renal proximal tubule cells.

机译:雌二醇17β刺激磷酸盐吸收,并且对原代兔肾近端小管细胞有丝分裂作用。

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摘要

The direct effects of estradiol-17beta (E(2)) on phosphate (P(i)) uptake and on DNA synthesis in the primary rabbit kidney proximal tubule cells (PTCs) have been investigated. In the present study, E(2) (>10(-9) M, over 9 days) causes an increase both in [(3)H]thymidine incorporation and the number of PTCs. The anti-estrogen tamoxifen completely prevented the E(2)-induced increase in [(3)H]thymidine incorporation, and ameliorated the stimulatory effect of E(2) on growth. E(2) (>10(-9 )M, over 5 days) also stimulated the P(i) uptake and its effect was due to the V(max) values but not to the K(m) value for P(i) uptake. Estriol and estrone also exerted significant stimulatory effects on P(i) uptake. Progesterone, tamoxifen, actinomycin D and cycloheximide prevented the E(2)-induced stimulation of P(i) uptake. In conclusion, estrogens at physiological concentrations stimulate P(i) uptake and DNA synthesis in the renal proximal tubule cells, and these effects are estrogen receptor mediated. Copyright 2002 S. Karger AG, Basel
机译:已经研究了雌二醇-17β(E(2))对磷酸盐(P(i))摄取和对主要兔肾近端小管细胞(PTC)中DNA合成的直接影响。在本研究中,E(2)(> 10(-9)M,超过9天)引起[(3)H]胸苷掺入和PTC数量的增加。抗雌激素他莫昔芬完全阻止E(2)诱导的[(3)H]胸苷掺入的增加,并改善了E(2)对生长的刺激作用。 E(2)(> 10(-9)M,超过5天)也刺激了P(i)的吸收,其作用是由于V(max)值而不是P(i)的K(m)值)摄取。雌三醇和雌酮也对P(i)的吸收产生显着的刺激作用。孕酮,他莫昔芬,放线菌素D和环己酰亚胺阻止了E(2)诱导的P(i)吸收刺激。总之,在生理浓度的雌激素刺激肾近端小管细胞中P(i)的摄取和DNA的合成,这些作用是雌激素受体介导的。版权所有2002 S. Karger AG,巴塞尔

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