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.
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.
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Raloxifene 加 17β-雌二醇 通过 janus 激酶/信号转导器和转录 3 级联激活剂抑制原代培养的血管平滑肌细胞和人乳腺内皮细胞的增殖。
DOI：
10.1016/j.ejphar.2007.01.026
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发表时间：
2007
影响因子：
5
通讯作者：
Yu Cui
中科院分区：
文献类型：
--
作者：
Ting;Qiuling Xiang;Jian Wen Chen;Hong Pan;Yu Cui
长期使用雌激素替代疗法会增加患乳腺癌的风险。目前，我们研究了第二代选择性雌激素受体调节剂雷洛昔芬和17 -雌二醇对原代培养血管平滑肌细胞（VSMC）和人乳腺内皮细胞（HMEC）增殖的影响及其机制。雷洛昔芬加17β -雌二醇抑制血管紧张素i诱导的VSMC增殖和STAT3的快速磷酸化；这些作用被janus kinase/signal transducer and activator of transcription3 (JAK/STAT3) inhibitor AG490阻断。stat3的生产没有受到影响。在原代培养的HMEC中，免疫荧光在细胞核中鉴定出erβ亚型，而没有erα亚型。雷洛昔芬加17 -雌二醇可抑制17 -雌二醇诱导的HMEC增殖。Western blot分析证实，雷洛昔芬可减弱17 β -雌二醇诱导的STAT3磷酸化，而这种作用可被AG490阻断。我们得出结论，雷洛昔芬加17 β -雌二醇通过JAK/ stat3级联抑制VSMC和HMEC的增殖，这可能是通过ERbeta在原代培养的HMEC中实现的。
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 angiotensinII-induced VSMC proliferation and rapid phosphorylation of STAT3; these effects were blocked by AG490, the janus kinase/signal transducer and activator of transcription3 (JAK/STAT3) inhibitor. STAT3production 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 STAT3, 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/STAT3cascade, which in primary cultured HMEC may be implemented through ERbeta.
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影响因子：
56.9
作者：
YU, CL;MEYER, DJ;JOVE, R
通讯作者：
JOVE, R
培养的主动脉平滑肌细胞中癌基因表达的调节。
DOI：
--
发表时间：
1986
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Kindy,MS;Sonenshein,GE
通讯作者：
Sonenshein,GE
影响因子：
8.7
作者：
Dubey, RK;Jackson, EK;Keller, PJ
通讯作者：
Keller, PJ
DOI：
10.1073/pnas.97.8.4227
发表时间：
2000-04-11
影响因子：
11.1
作者：
Grandis, JR;Drenning, SD;Kim, JD
通讯作者：
Kim, JD