17beta-estradiol prevents programmed cell death in cardiac myocytes.
17beta-estradiol prevents programmed cell death in cardiac myocytes.
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17β-雌二醇可防止心肌细胞程序性细胞死亡。
DOI：
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发表时间：
2000
期刊：
影响因子：
--
通讯作者：
L. Neyses
中科院分区：
文献类型：
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作者：
T. Pelzer;Michael Schumann;M. Neumann;Tertia deJager;M. Stimpel;E. Serfling;L. Neyses
雌激素的心脏保护作用是明确的。然而，人们对其潜在的机制知之甚少。由于细胞程序性死亡(细胞凋亡)可能是心力衰竭时心肌细胞丢失的原因，而且雌激素可以阻止乳腺癌细胞的凋亡，我们研究了生理剂量的17β-雌二醇是否可以预防由细胞程序性死亡引起的心肌细胞损失。用星形孢子素诱导培养的心肌细胞发生凋亡。17β-雌二醇(10 NM)具有抗细胞凋亡作用，通过形态分析、Hoechst染料33342活染色和末端转移酶dUTP缺口末端标记法(TUNEL)证实。作为17β-雌二醇抗细胞凋亡作用的一个潜在机制，我们发现在激素处理的心肌细胞中ICE样蛋白酶caspase-3的活性降低。此外，雌激素抑制细胞凋亡与核因子-kappaB转录因子活性降低有关，尤其是p65/relA和p50。据我们所知，这些数据提供了生理浓度的17β-雌二醇抑制心肌细胞凋亡的第一个迹象。雌激素的抗细胞凋亡作用可能有助于已知的雌激素的心脏保护作用，并为未来治疗方案的发展提供了一个起点。
The cardioprotective effects of estrogens are clearly established. However, the underlying mechanisms are poorly understood. Because programmed cell death (apoptosis) probably contributes to the loss of cardiac myocytes in heart failure and because estrogens prevent apoptosis in breast cancer cells, we investigated whether the loss of cardiac myocytes by programmed cell death could be prevented by physiological doses of 17beta-estradiol. Apoptosis of cultured cardiac myocytes was induced by staurosporine. 17beta-estradiol (10 nM) had an antiapoptotic effect as determined by morphological analysis, vital staining using the Hoechst dye 33342 and terminal transferase dUTP nick-end labeling (TUNEL). As a potential mechanism for the antiapoptotic effect of 17beta-estradiol we found a reduced activity of the ICE-like protease caspase-3 in hormone-treated myocytes. Furthermore, inhibition of apoptosis by estradiol was associated with a reduced activity of NF-kappaB transcription factors, particularly p65/RelA and p50. To our knowledge, these data provide the first indication that 17beta-estradiol in physiological concentrations inhibits apoptosis in cardiac myocytes. The antiapoptotic effect of estrogens might contribute to the known cardioprotective effect of estrogens and provides a starting point for the development of future treatment options.
DOI：
10.1097/00006254-199202000-00027
发表时间：
1991-09
期刊：
The New England journal of medicine
影响因子：
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作者：
M. Stampfer;G. Colditz;W. Willett;J. Manson;B. Rosner;F. Speizer;C. Hennekens
通讯作者：
M. Stampfer;G. Colditz;W. Willett;J. Manson;B. Rosner;F. Speizer;C. Hennekens