雌激素受体及其介导的血管保护作用

雌激素的生物学效应是由雌激素受体所介导 ,血管壁中存在有雌激素受体 ,为雌激素对血管的直接作用提供了分子水平的物质基础。本文介绍了雌激素受体的结构和特性、雌激素受体亚型、雌激素作用机制、膜雌激素受体及血管壁雌激素受体及其介导的血管保护作用     

雌激素受体与心血管保护作用

雌激素具有抗动脉粥样硬化作用 ,雌激素受体主要是通过抑制血管平滑肌细胞增殖和迁移以及促进内皮细胞释放一氧化氮而介导了这一保护效应。研究雌激素受体的作用机制 ,有助于深入了解雌激素的心血管保护效应 ,为绝经期妇女雌激素替代治疗乃至冠心病的预防治疗提供理论依据。     

雌激素对血管、心肌保护性作用的分子机制

雌激素具有调节血管功能、保护内皮、抗动脉粥样硬化、抑制血管钙化、调节心肌电活动和抑制心肌细胞凋亡等作用,在预防心血管疾病方面具有重要的临床价值。雌激素可产生复杂的生物学效应,其保护作用机制涉及较多的信号通路,如丝裂原活化蛋白激酶途径、磷脂酰肌醇-3激酶/蛋白激酶B途径和骨保护素/核因子κB受体活化因子配体途径等。该文主要介绍雌激素对血管内皮、血管平滑肌和心肌的保护性作用的分子机制。     

雌激素受体与心血管保护作用

雌激素具有抗动脉粥样硬化作用,雌激素受体主要是通过抑制血管平滑肌细胞增殖和迁移以及促进内皮细胞释放一氧化氮而介导了这一保护效应,研究雌激素受体的作用机制,有助于深入了解雌激素的心血管保护效,应,为绝经期妇女雌激素替代治疗乃至冠心病的预防治疗提供理论依据。     

雌激素对血管保护的机制探讨

雌激素除对女性的心血管系统具有保护外,还作用于血管的组成部分内皮细胞和平滑肌细胞.本文探讨雌激素通过对血管的作用维持内皮细胞功能和抑制平滑肌细胞的移行,从而起心血管保护的细胞、分子机制.     

雌激素对肺血管的保护作用

自发现雌激素有预防动脉粥样硬化和冠心病的作用以来，有关雌激素作用机制的研究多集中在雌激素与血脂代谢及与血管壁的直接作用方面。但统计学分析认为，雌激素对动脉粥样硬化的作用50％～70％源于非脂质因素。此前大多数研究集中在雌激素及其受体对体循环血管的保护作用，对肺血管的作用研究较少，其机制有待进一步探讨。本文就近年来有关的研究进展进行综述。     

雌激素对血管保护的机制探讨

雌激素除对女性的心血管系统具有保护外,还作用于血管的组成部分内皮细胞和平滑肌细胞.本文探讨雌激素通过对血管的作用维持内皮细胞功能和抑制平滑肌细胞的移行,从而起心血管保护的细胞、分子机制.     

雌激素保护缺血性脑损害的分子机制

大量研究表明,雌激素对缺血性脑损伤具有保护作用,其机制相当复杂,涉及多个方面。文章就近年来雌激素对神经元、胶质细胞和血管三个方面的保护作用及其分子机制的研究进展进行综述。     

雌激素保护缺血性脑损害的分子机制

大量研究表明，雌激素对缺血性脑损伤具有保护作用，其机制相当复杂，涉及多个方面。文章就近年来雌激素对神经元、胶质细胞和血管三个方面的保护作用及其分子机制的研究进展进行综述。     

雌激素在心血管系统中保护作用的研究进展

雌激素在心血管系统中的作用一直是人们所关注的问题 ,而雌激素替代治疗的应用价值亦成为目前研究的热点。众所周知 ,男性和女性之间的心血管疾病的发病率有着显著性差异 ,在某种程度上与两者之间的易患因素和激素水平的不同有关 [1]。动脉粥样硬化病变在绝经前期的妇女中发病率较低 ,而在绝经后则升高。以往认为雌激素的动脉保护作用归因于对血脂浓度的调节 ;而有研究发现血清中雌激素诱导脂类的变化 ,仅占临床观察到的雌激素有益作用的 1/ 3,因为雌激素的心血管保护作用实际上是通过血管中的雌激素被激活而发挥作用[2 ] 。目前认为血管与…     

Neuroprotection mediated through estrogen receptor-alpha in astrocytes

Estrogen has well-documented neuroprotective effects in a variety of clinical and experimental disorders of the CNS, including autoimmune inflammation, traumatic injury, stroke, and neurodegenerative diseases. The beneficial effects of estrogens in CNS disorders include mitigation of clinical symptoms, as well as attenuation of histopathological signs of neurodegeneration and inflammation. The cellular mechanisms that underlie these CNS effects of estrogens are uncertain, because a number of different cell types express estrogen receptors in the peripheral immune system and the CNS. Here, we investigated the potential roles of two endogenous CNS cell types in estrogen-mediated neuroprotection. We selectively deleted estrogen receptor-α (ERα) from either neurons or astrocytes using well-characterized Cre-loxP systems for conditional gene knockout in mice, and studied the effects of these conditional gene deletions on ERα ligand-mediated neuroprotective effects in a well-characterized model of adoptive experimental autoimmune encephalomyelitis (EAE). We found that the pronounced and significant neuroprotective effects of systemic treatment with ERα ligand on clinical function, CNS inflammation, and axonal loss during EAE were completely prevented by conditional deletion of ERα from astrocytes, whereas conditional deletion of ERα from neurons had no significant effect. These findings show that signaling through ERα in astrocytes, but not through ERα in neurons, is essential for the beneficial effects of ERα ligand in EAE. Our findings reveal a unique cellular mechanism for estrogen-mediated CNS neuroprotective effects by signaling through astrocytes, and have implications for understanding the pathophysiology of sex hormone effects in diverse CNS disorders.     

Suppression of estrogen actions in human lung cancer

Estrogen plays a critical role in female reproduction but has also been reported to have important roles in various target tissues expressing estrogen receptor (ER) α and/or ERβ in both male and female. ERs especially ERβ have been demonstrated to be present and functional in both normal human lung and its disorders including cancer. Non-small cell lung carcinomas (NSCLCs) are well-known to be composed of heterogeneous groups. Squamous cell carcinoma is the most common subtype in men, but adenocarcinoma is the most common histologic subtype in women. Therefore, sex steroid hormones such as estrogens have been considered to play some roles in NSCLC. In particular, results of several epidemiological analyses pointed out the association between physiological or artificial alterations of hormone status such as menstruation and postmenopausal administration of hormone replacement therapy and lung cancer risks or its development especially in female subjects. In NSCLC tissues, intratumoral estrogen synthesis via aromatase, which is a key enzyme in the estrogen synthesis involved in aromatization of androgens into estrogens, has recently become of clinical interest as a possible target of therapy. Therefore, in this review, we focused on the potential of an endocrine therapy in NSCLC using clinically available inhibitors of estrogen and aromatase actions.     

Estrogen receptor beta is involved in the anorectic action of estrogen

OBJECTIVE: Estrogen has been implicated in feeding behavior and adiposity. This study was undertaken to elucidate the mechanism underlying the anti-obesity and anorectic action of estrogen and the role of estrogen receptor (ER) in the central nervous system. METHODS AND RESULTS: Ovariectomy in 8-week-old female Wistar rats induced hyperphagia along with an increase in body weight and abdominal fat accumulation compared to control sham-operated rats. These changes were fully reversed by subcutaneous replacement of estradiol and were abrogated by pair-feeding. Then, the effects of intracerebroventricular infusion of estradiol, alone or in combination with antisense oligodeoxynucleotides (ODN), for ER in ovariectomized rats were examined. The estradiol group showed 10-20% lower daily food intake, and after the 2-week infusion period a 14% reduction in body weight with a similar reduction in abdominal fat compared to the vehicle group. The inhibitory effect of estradiol on food intake and body weight was blocked by co-administration of ER-beta antisense ODN, whereas ER-alpha antisense ODN did not show any influence. CONCLUSION: These results indicate that ER-beta in the central nervous system is involved in the anorectic action of estrogen.