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首页> 外文期刊>Cell biology international. >Regulation of osteogenesis of human amniotic mesenchymal stem cells by sodium butyrate
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Regulation of osteogenesis of human amniotic mesenchymal stem cells by sodium butyrate

机译:用丁酸钠调节人羊膜间充质干细胞的骨质发生

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Abstract Human amniotic membrane‐derived mesenchymal stem cells (hAMSCs) draw great interests for regenerative medicine due to convenient availability and low immunogenicity. However, suboptimal culture conditions limit their application. In recent years, small molecules have proven powerful in regulating stem cell fates and can be applied to stimulate their function. In the present study, the impacts of sodium butyrate (NaBu), a histone deacetylase inhibitor (HDACi), on hAMSCs were investigated. It was shown that NaBu at a low concentration inhibited cell proliferation by arresting cell cycle at G0/G1 rather than inducing apoptosis. When NaBu was supplemented at a concentration of 1.0?mM for 3 days during osteogenic induction, significantly more mineralized nodules were generated and the expression of osteogenesis‐related genes ( ALP , Runx2 , Opn , and Ocn ) and proteins (Col1a1, OPN, OCN, Runx2, and TAZ) were both significantly enhanced. However, a higher concentration (1.0?mM) and longer exposure time (14 days) of NaBu showed no such effects, which may be partially attributed to both the increased expression of histone deacetylase 8 (HDAC8) and reduced level of H3K9‐Ace, thus leading to the transcriptional inhibition during osteogenesis. Further, it was indicated that ERK might be involved in the stimulatory effects of NaBu. These findings may be helpful to develop an efficient culture process for hAMSCs towards bone regeneration.
机译:摘要由于方便的可用性和低免疫原性,摘要人羊膜衍生的间充质干细胞(Hamscs)为再生药引起了极大的兴趣。但是,次优文化条件限制了其申请。近年来,小分子已被证明是强大的调节干细胞命运,可以应用于刺激其功能。在本研究中,研究了HAMSCs上的丁酸钠(NaBU)(NaBU)的影响,组蛋白脱乙酰酶抑制剂(HDACI)。结果表明,低浓度下的NaBu通过在G0 / G1的细胞周期而不是诱导细胞凋亡时抑制细胞增殖。当NaBu以浓度补充浓度的浓度,在成骨诱导期间3天,产生了更大的矿化结节,并表达了与骨开发相关基因(ALP,RUNX2,OPN和OCN)和蛋白质(COL1A1,OPN) ,OCN,Runx2和TAZ)既明显增强。然而,更高的浓度(1.0μm)和更长的Nabu暴露时间(14天)显示出没有这种作用,其可以部分地归因于组蛋白脱乙酰酶8(HDAC8)的增加和H3K9-Ace的降低水平的表达。因此导致骨质发生过程中的转录抑制。此外,结果表明ERK可能参与NABU的刺激作用。这些调查结果可能有助于为HAMSCS开发高效的培养过程对骨再生。

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