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首页> 外文期刊>Cell and Tissue Research >Estradiol effects on intracellular Ca2+ homeostasis in bovine brain-derived endothelial cells
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Estradiol effects on intracellular Ca2+ homeostasis in bovine brain-derived endothelial cells

机译：雌二醇对牛脑源性内皮细胞内Ca 2 + 稳态的影响

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Estrogens diversely affect various physiological processes by genomic or non-genomic mechanisms, in both excitable and non-excitable cells. Additional to the trophic effects of estrogens promoting cell growth and differentiation, recent experimental evidence highlights their involvement in the regulation of intracellular Ca2+ homeostasis. The effects of estrogens on excitable cells are well documented. However, these steroids also influence numerous physiological events in non-excitable cells, such as fibroblasts or vascular endothelial cells. We have focused our attention on an immortalized endothelial-like cell line derived from fetal bovine cerebellum. Estradiol (E2) effects on intracellular Ca2+ homeostasis were tested by varying the exposure time to the hormone (8, 24, 48 h). Calcium measurements were performed with genetically encoded Ca2+ probes (Cameleons) targeted to the main subcellular compartments involved in intracellular Ca2+ homeostasis (cytosol, endoplasmic reticulum, mitochondria). Mitochondrial Ca2+ uptake significantly decreased after 48-h exposure to E2, whereas cytosolic and endoplasmic reticulum responses were unaffected. The effect of E2 on mitochondrial Ca2+ handling was blocked by ICI 182,780, a pure estrogen receptor antagonist, suggesting that the effect was estrogen-receptor–mediated. To evaluate whether the decrease of Ca2+ uptake affected mitochondrial membrane potential (ΔΨm), cells were monitored in the presence of tetra-methyl-rhodamine-methylester; no significant changes were seen between cells treated with E2 and controls. To investigate a mechanism of action, we assessed the possibile involvement of the permeability transition pore (PTP), an inner mitochondrial membrane channel influencing energy metabolism and cell viability. We treated cells with CyclosporinA (CsA), which binds to the matrix chaperone cyclophilin-D and regulates PTP opening. CsA reversed the effects of a 48-h treatment with E2, suggesting a possible transcriptional modulation of proteins involved in the mitochondrial permeability transition process.
机译：雌激素通过基因组或非基因组机制在可激发和不可激发的细胞中多种多样地影响各种生理过程。除了雌激素促进细胞生长和分化的营养作用外，最近的实验证据还表明，雌激素参与细胞内Ca 2 + 稳态的调节。雌激素对可兴奋细胞的作用已有充分文献记载。但是，这些类固醇还影响非兴奋性细胞（例如成纤维细胞或血管内皮细胞）中的许多生理事件。我们将注意力集中在源自胎牛小脑的永生化内皮样细胞系上。通过改变激素暴露时间（8、24、48 h）来测试雌二醇（E 2 ）对细胞内Ca 2 + 体内稳态的影响。用基因编码的Ca 2 + 探针（Cameleons）对钙进行测量，这些探针靶向参与细胞内Ca 2 + 体内稳态（细胞质，内质网，线粒体）的主要亚细胞区室。暴露于E 2 48小时后，线粒体Ca 2 + 的摄取显着降低，而胞质和内质网反应未受影响。 E 2 对线粒体Ca 2 + 处理的作用被ICI 182,780（一种纯雌激素受体拮抗剂）阻断，表明该作用是雌激素受体介导的。为了评估Ca 2+摄取的减少是否影响线粒体膜电位（ΔΨm），在四甲基罗丹明甲酯存在下监测细胞。用E 2 处理的细胞与对照之间未见明显变化。为了研究作用机制，我们评估了通透性过渡孔（PTP），影响能量代谢和细胞活力的内部线粒体膜通道的可能参与。我们用CyclosporinA（CsA）处理细胞，该细胞与基质分子伴侣亲环蛋白-D结合并调节PTP的开放。 CsA逆转了用E 2 处理48小时的效果，表明可能参与线粒体通透性转变过程的蛋白质的转录调控。

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