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  • Title: Raloxifene plus 17beta-estradiol inhibits proliferation of primary cultured vascular smooth muscle cells and human mammary endothelial cells via the janus kinase/signal transducer and activator of transcription3 cascade.
    Author: Wang TH, Xiang QL, Chen JW, Pan H, Cui YH.
    Journal: Eur J Pharmacol; 2007 Apr 30; 561(1-3):7-13. PubMed ID: 17336289.
    Abstract:
    Long-term use of estrogen replacement therapy increases the risk of breast cancer. Presently, we investigated the effects and mechanisms of Raloxifene, a second generation selective estrogen receptor modulator, plus 17beta-estradiol on the proliferation of primary cultured vascular smooth muscle cells (VSMC) and human mammary endothelial cells (HMEC). Raloxifene plus 17beta-estradiol inhibited angiotensin II-induced VSMC proliferation and rapid phosphorylation of STAT(3); these effects were blocked by AG490, the janus kinase/signal transducer and activator of transcription3 (JAK/STAT(3)) inhibitor. STAT(3) production was not affected. In primary cultured HMEC, immunofluorescence identified the ERbeta subtype, but not the ERalpha subtype, in the nucleus. Raloxifene plus 17beta-estradiol inhibited 17beta-estradiol-induced proliferation of HMEC. Western blot analysis established that Raloxifene attenuated the 17beta-estradiol-induced phosphorylation of STAT(3), and that this effect was blocked by AG490. We conclude that Raloxifene plus 17beta-estradiol inhibits the proliferation of VSMC and HMEC through the JAK/STAT(3) cascade, which in primary cultured HMEC may be implemented through ERbeta.
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