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首页> 外文期刊>Biochemical and Biophysical Research Communications >Nicotine induces cell proliferation in association with cyclin D1 up-regulation and inhibits cell differentiation in association with p53 regulation in a murine pre-osteoblastic cell line.
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Nicotine induces cell proliferation in association with cyclin D1 up-regulation and inhibits cell differentiation in association with p53 regulation in a murine pre-osteoblastic cell line.

机译:在鼠成骨细胞前体细胞系中,尼古丁与细胞周期蛋白D1上调相关联诱导细胞增殖,并与p53调控相关联抑制细胞分化。

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摘要

Recent studies have suggested that nicotine critically affects bone metabolism. Many studies have examined the effects of nicotine on proliferation and differentiation, but the underlying molecular mechanisms remain unclear. We examined cell cycle regulators involved in the proliferation and differentiation of MC3T3-E1 cells. Nicotine induced cell proliferation in association with p53 down-regulation and cyclin D1 up-regulation. In differentiated cells, nicotine reduced alkaline phosphatase activity and mineralized nodule formation in dose-dependent manners. Furthermore, p53 expression was sustained in nicotine-treated cells during differentiation. These findings indicate that nicotine promotes the cell cycle and inhibits differentiation in association with p53 regulation in pre-osteoblastic cells.
机译:最近的研究表明,尼古丁会严重影响骨骼代谢。许多研究已经检查了尼古丁对增殖和分化的影响,但潜在的分子机制仍不清楚。我们检查了参与MC3T3-E1细胞增殖和分化的细胞周期调节剂。尼古丁诱导的细胞增殖与p53下调和细胞周期蛋白D1上调相关。在分化的细胞中,尼古丁以剂量依赖的方式降低了碱性磷酸酶的活性并降低了矿化结节的形成。此外,在分化过程中在烟碱处理的细胞中p53表达得以维持。这些发现表明烟碱促进成骨细胞前细胞中的细胞周期并抑制与p53调控相关的分化。

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