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磷脂酰肌醇-3激酶(PI3K)可能参与催乳素刺激的小鼠乳腺外植体中乳产物形成和碘转运过程。

Possible involvement of P13K in prolactin-stimulated milk product formation and iodide transport in mouse mammary explants.

作者信息

Hang J, Rillema J A

机构信息

Department of Physiology, School of Medicine, Wayne State University, Detroit, Michigan 48201, USA.

出版信息

Proc Soc Exp Biol Med. 1998 Nov;219(2):154-9. doi: 10.3181/00379727-219-44329.

DOI:10.3181/00379727-219-44329
PMID:9790174
Abstract

The in vitro effect of wortmannin, an inhibitor of P13 kinase, on prolactin (PRL) stimulated p70S6K, iodide transport, and milk product synthesis were investigated in cultured mouse mammary tissues. Mouse mammary gland explants were initially incubated for 24 hr in media M199 containing 1 microg/ml insulin and 10(-7)M cortisol. A subsequent treatment with wortmannin impeded, in a dose-dependent fashion, the PRL stimulation of casein, lipid, and lactose synthesis as well as the PRL stimulation of iodide transport. Rapamycin (25 ng/ml), an inhibitor of p70S6K, also inhibited the effect of PRL on iodide transport; this drug was earlier shown to inhibit PRL effects on milk product synthesis. These results suggest the possible involvement of p70S6K and P13-kinase in PRL-stimulated milk product formation and iodide transport in mouse mammary explants. Since wortmannin caused a diminished cellular content of p70S6K and a reduced extent of P70S6K migration in polyacrylamide gels (likely due to dephosphorylation), P13-kinase likely lies upstream in the PRL signaling pathway for p70S6K activation.

摘要

研究了磷脂酰肌醇-3激酶(PI3激酶)抑制剂渥曼青霉素对培养的小鼠乳腺组织中催乳素(PRL)刺激的p70S6K、碘转运和乳产品合成的体外作用。小鼠乳腺外植体最初在含有1微克/毫升胰岛素和10^(-7)摩尔/升皮质醇的M199培养基中孵育24小时。随后用渥曼青霉素处理以剂量依赖性方式阻碍了PRL对酪蛋白、脂质和乳糖合成的刺激以及PRL对碘转运的刺激。雷帕霉素(25纳克/毫升),一种p70S6K抑制剂,也抑制了PRL对碘转运的作用;该药物 earlier 已被证明可抑制PRL对乳产品合成的作用。这些结果表明p70S6K和PI3激酶可能参与了PRL刺激的小鼠乳腺外植体中乳产品形成和碘转运。由于渥曼青霉素导致p70S6K的细胞含量减少以及p70S6K在聚丙烯酰胺凝胶中的迁移程度降低(可能是由于去磷酸化),PI3激酶可能在PRL信号通路中位于p70S6K激活的上游。

注

“earlier”原文有误,推测是“earlier”,暂按此翻译,具体需结合正确原文确定准确意思。

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