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首页> 外文期刊>Cell cycle >Unraveling estrogen action in osteoporosis.
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Unraveling estrogen action in osteoporosis.

机译：阐明雌激素在骨质疏松症中的作用。

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摘要

A decrease in estrogen levels at menopause leads to a rapid loss of bone mineral density and an increase in fracture risk. For over ten years it has been known that the beneficial effects of estrogen are due in part to the ability of estrogen to suppress osteoclastogenic cytokine production in T-cells and osteoblasts. In addition to suppressing these cytokines, estrogen has been shown to induce the apoptotic death of osteoclasts. A variety of different mechanisms have been suggested to explain the estrogen regulation of osteoclast survival. One hypothesis is that estrogen, via rapid non-genomic signaling, induces apoptosis without the need for direct binding of estrogen receptor alpha (ERalpha) to DNA. A second hypothesis proposes that estrogen-stimulation of ERalpha in osteoclasts induces the expression Fas Ligand which in turn leads to cell death via an autocrine mechanism. In contrast, recent work from our lab has led to a genomic model of estrogen action in which estrogen acts to induce ERalpha binding to transcriptional enhancers in the Fas Ligand gene leading to its upregulation in osteoblasts which through a paracrine mechanism induces apoptosis in osteoclasts. Here we will focus on these differing models of the mechanism of estrogen-mediated osteoclast apoptosis.
机译：绝经期雌激素水平的降低导致骨矿物质密度的快速损失和骨折风险的增加。十多年来，已知雌激素的有益作用部分归因于雌激素抑制T细胞和成骨细胞中破骨细胞生成细胞因子的能力。除抑制这些细胞因子外，雌激素还显示出诱导破骨细胞凋亡的作用。已经提出了多种不同的机制来解释破骨细胞存活的雌激素调节。一种假设是雌激素通过快速的非基因组信号传导诱导凋亡，而无需将雌激素受体α（ERalpha）与DNA直接结合。第二个假设提出破骨细胞中ERα的雌激素刺激诱导表达Fas配体，其进而通过自分泌机制导致细胞死亡。相反，我们实验室的最新工作导致了雌激素作用的基因组模型，其中雌激素起诱导ERalpha结合Fas Ligand基因中转录增强子的作用，从而导致其在成骨细胞中上调，并通过旁分泌机制诱导破骨细胞凋亡。在这里，我们将专注于这些不同的雌激素介导的破骨细胞凋亡机制的模型。

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