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J Dent Res：MSC中过表达的Sirt1促进Bmi1缺陷小鼠中的牙本质形成

2019-03-25 不详 网络

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Sirt1促进人牙髓细胞中的成牙本质细胞基因表达，而Sirt1的抑制下调这些基因的表达。为了研究由Prx1启动子驱动的间充质干细胞（MSCs）中Sirt1的过表达是否可以挽救Bmi1缺陷型（Bmi1-/-）小鼠的牙本质形成缺陷，我们在Bmi1敲除小鼠（Sirt1TGBmi1-/-）中建立了过表达Sirt1的MSCs。首先，我们使用Prx1-Cre/ROSAnTnG小鼠来证明Prx1系细胞主要存在于

Sirt1促进人牙髓细胞中的成牙本质细胞基因表达，而Sirt1的抑制下调这些基因的表达。为了研究由Prx1启动子驱动的间充质干细胞（MSCs）中Sirt1的过表达是否可以挽救Bmi1缺陷型（Bmi1-/-）小鼠的牙本质形成缺陷，我们在Bmi1敲除小鼠（Sirt1TGBmi1-/-）中建立了过表达Sirt1的MSCs。

首先，我们使用Prx1-Cre/ROSAnTnG小鼠来证明Prx1系细胞主要存在于4周龄的牙髓中。其次，我们发现与野生型（WT）小鼠相比，4周龄的Sirt1TG小鼠牙齿体积增加。Sirt1的表达水平在Sirt1TG小鼠的牙乳头间充质细胞中明显高于WT小鼠。此外，我们证明Sirt1TG小鼠的牙齿矿化，牙齿体积，牙本质涎蛋白免疫阳性区域，成牙本质细胞基因表达和增殖BrdU阳性细胞百分比显著升高，而Bmi1-/-小鼠与WT小鼠相比显著降低。然而，与WT小鼠相比，Sirt1TG小鼠中prentin的面积和TUN小鼠EL阳性凋亡细胞的百分比显著降低，但在Bmi1-/-小鼠中明显增加。所有这些参数都在Sirt1TG Bmi1-/-小鼠和Bmi1-/-小鼠中拯救。最后，通过使用牙乳头间充质细胞，我们发现Sirt1的过表达挽救了细胞增殖和分化的减少，并增加了Bmi1缺乏引起的细胞凋亡，这与p53脱乙酰化增加有关。

因此，本研究表明，Sirt1是一种潜在的治疗靶点，用于促进牙本质形成的合成代谢方法治疗牙齿发育缺陷。

原始出处：

Wang H, Lv C, et al., Overexpressed Sirt1 in MSCs Promotes Dentin Formation in Bmi1-Deficient Mice. J Dent Res. 2018 Nov;97(12):1365-1373. doi: 10.1177/0022034518781509. Epub 2018 Jun 22.

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    2019-04-01 lq1767

    #过表达#

    0

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    2019-03-27 huanbaofeng

    #MSC#

    0

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    2019-03-27 ms8538335253054589

    #牙本质#

    0

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    2019-03-27 quxin068

    #sirt1#

    0