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首页> 美国卫生研究院文献>other >Estrogen Receptor (ER)-α36 Is Involved in Estrogen- and Tamoxifen-Induced Neuroprotective Effects in Ischemic Stroke Models
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Estrogen Receptor (ER)-α36 Is Involved in Estrogen- and Tamoxifen-Induced Neuroprotective Effects in Ischemic Stroke Models

机译：在缺血性卒中模型中雌激素受体（ER）-α36参与雌激素和他莫昔芬诱导的神经保护作用

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摘要

The neuroprotection by estrogen (E2) and tamoxifen is well documented in experimental stroke models; however, the exact mechanism is unclear. A membrane-based estrogen receptor, ER-α36, has been identified. Postmenopausal-levels of E2 act through ER-α36 to induce osteoclast apoptosis due to a prolonged activation of the mitogen-activated protein kinase (MAPK)/extracellular signal-related kinase (ERK) signaling. We hypothesized that ER-α36 may play a role in the neuroprotective activities of estrogen and tamoxifen. Here, we studied ER-α36 expression in the brain, as well as its neuroprotective effects against oxygen and glucose deprivation (OGD) in PC12 cells. We found that ER-α36 was expressed in both rat and human brain. In addition, OGD-induced cell death was prevented by l nmol/L 17β-estradiol (E2β). E2β activates the MAPK/ERK signaling pathway in PC12 cells under basal and OGD conditions by interacting with ER-α36 and also induces ER-α36 expression. Low-dose of tamoxifen up-regulated ER-α36 expression and enhanced neuronal survival in an ovariectomized ischemic stroke model. Furthermore, low-dose of tamoxifen enhanced neuroprotective effects by modulating activates or suppress ER-α36. Our results thus demonstrated that ER-α36 is involved in neuroprotective activities mediated by both estrogen and tamoxifen.
机译：在实验性卒中模型中，雌激素（E2）和他莫昔芬对神经的保护作用已得到充分证明。但是，确切的机制尚不清楚。已经鉴定出基于膜的雌激素受体ER-α36。绝经后水平的E2通过ER-α36发挥作用，从而导致破骨细胞凋亡，这是由于促分裂原激活的蛋白激酶（MAPK）/细胞外信号相关激酶（ERK）信号的延长激活所致。我们假设ER-α36可能在雌激素和他莫昔芬的神经保护活性中起作用。在这里，我们研究了ER-α36在大脑中的表达及其对PC12细胞中氧和葡萄糖剥夺（OGD）的神经保护作用。我们发现ER-α36在大鼠和人脑中均表达。另外，l nmol / L17β-雌二醇（E2β）可防止OGD诱导的细胞死亡。 E2β通过与ER-α36相互作用，在基础和OGD条件下激活PC12细胞中的MAPK / ERK信号通路，并诱导ER-α36表达。在卵巢切除的缺血性卒中模型中，小剂量的他莫昔芬上调ER-α36表达并增强神经元存活。此外，低剂量的他莫昔芬通过调节激活或抑制ER-α36增强神经保护作用。因此，我们的结果表明，ER-α36参与由雌激素和他莫昔芬介导的神经保护活性。

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