雌二醇-17 β刺激磷酸盐摄取,对原代兔肾近端小管细胞有丝分裂作用。

Ho Jae Han, Yeune Hee Lee, Kwon Moo Park, Mary Taub
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引用次数: 9

摘要

研究了雌二醇-17 β (E(2))对原代兔肾近端小管细胞(ptc)中磷酸(P(i))摄取和DNA合成的直接影响。在本研究中,E(2) (>10(-9) M,超过9天)导致[(3)H]胸腺嘧啶掺入和ptc数量增加。抗雌激素的他莫昔芬完全阻止了E(2)诱导的[(3)H]胸腺嘧啶掺入增加,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)吸收的K(M)值。雌三醇和雌酮对P(i)的摄取也有显著的刺激作用。黄体酮、他莫昔芬、放线菌素D和环己亚胺阻止了E(2)诱导的P(i)摄取刺激。综上所述,生理浓度的雌激素刺激肾近端小管细胞P(i)的摄取和DNA的合成,这些作用是由雌激素受体介导的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Estradiol-17beta stimulates phosphate uptake and is mitogenic for primary rabbit renal proximal tubule cells.

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.

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