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首页> 外文期刊>Journal of Cellular Physiology >Upregulation of Runt-Related Transcription Factor-2 Through CCAAT Enhancer Binding Protein-beta Signaling Pathway in Microglial BV-2 Cells Exposed to ATP
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Upregulation of Runt-Related Transcription Factor-2 Through CCAAT Enhancer Binding Protein-beta Signaling Pathway in Microglial BV-2 Cells Exposed to ATP

机译：Upregulation Runt-Related转录的因子2通过CCAAT增强器绑定在小胶质BV-2 Protein-beta信号通路细胞暴露于ATP

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摘要

We have shown constitutive expression of the master regulator of osteoblastogenesis, runt-related transcription factor-2 (Runx2), by microglia cells outside bone. Here, we attempted to evaluate the pathological significance of Runx2 in microglial BV-2 cells exposed to ATP at a high concentration. Marked upregulation of Runx2 transcript and protein expression was seen in cells exposed to 1 mM ATP for a period longer than 30 min without inducing cytotoxicity. The Runx2 upregulation by ATP was prevented by extracellular and intracellular Ca2+ chelators, while thapsigargin upregulated Runx2 expression alone without affecting the upregulation by ATP. A calmodulin antagonist prevented the upregulation by ATP, with calcineurin inhibitors being ineffective. Although ATP markedly increased nuclear levels of nuclear factor of activated T cell-2 (NFAT2), Runx2 promoter activity was not simulated by the introduction of either NFAT1 or NFAT2, but facilitated by that of CCAAT enhancer binding protein-alpha (C/EBP alpha), C/EBP beta and nuclear factor (erythroid-derived 2)-like-2 (Nrf2). Exposure to ATP up-regulated C/EBP beta and Nrf2, but not C/EBP alpha, expression, in addition to increasing nuclear levels of respective corresponding proteins. Runx2 upregulation by ATP was deteriorated by knockdown of C/EBP beta but not by that of Nrf2, however, while exposure to ATP up-regulated matrix metalloproteinase-13 (Mmp13) expression in a Runx2-dependent manner. Overexpression of Runx2 up-regulated Mmp13 expression with promoted incorporation of fluorescent beads into BV-2 cells without ATP. These results suggest that extracellular ATP up-regulates Runx2 expression through activation of the C/EBP beta signaling in a calmodulin-dependent manner to play a pivotal role in phagocytosis in microglial BV-2 cells. (C) 2015 Wiley Periodicals, Inc.
机译：我们展示了组成型表达的osteoblastogenesis主监管机构,runt-related转录因子2 (Runx2)小神经胶质细胞外骨。评估的病理意义Runx2小胶质BV-2细胞暴露于ATP高的浓度。Runx2转录和蛋白表达在细胞暴露于1毫米ATP的时间比30分钟没有诱导细胞毒性。Runx2 upregulation ATP阻止了细胞外和细胞内钙离子螯合剂,虽然thapsigargin调节Runx2的表达式孤独而不影响upregulation ATP。钙调素拮抗剂阻止了upregulation ATP,与钙调磷酸酶抑制剂是无效的。增加核的核转录因子的水平激活T电池2 (NFAT2), Runx2启动子活动并不是模拟的介绍NFAT1或NFAT2,但推波助澜的CCAAT增强器绑定protein-alpha (C / EBPα),C / EBPβ和核因子(erythroid-derived 2)如2 (Nrf2)。ATP上调C / EBPβ和Nrf2,但不是C / EBPα,表情,除了增加核的各自的水平相应的蛋白质。被击倒的C / EBPβ恶化但不是由Nrf2,然而,虽然接触ATP上调矩阵metalloproteinase-13(Mmp13) Runx2-dependent的方式表达。超表达Mmp13表达Runx2上调表达与提升的荧光珠成BV-2细胞ATP。这些结果表明,细胞外ATP通过激活让Runx2表达式的C / EBPβ信号calmodulin-dependent方式发挥的关键在小胶质BV-2细胞吞噬作用。(C) 2015年威利期刊公司。

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