留言板

尊敬的读者、作者、审稿人, 关于本刊的投稿、审稿、编辑和出版的任何问题, 您可以本页添加留言。我们将尽快给您答复。谢谢您的支持!

姓名
邮箱
手机号码
标题
留言内容
验证码
x

组蛋白去乙酰化酶在口腔来源成体干细胞成骨向/成牙本向分化的研究进展

宋词,  陈婷,  吴补领

downloadPDF
文章导航 > 分子影像学杂志  > 2019 >  42(2): 234-237
宋词, 陈婷, 吴补领. 组蛋白去乙酰化酶在口腔来源成体干细胞成骨向/成牙本向分化的研究进展[J]. 分子影像学杂志, 2019, 42(2): 234-237. doi: 10.12122/j.issn.1674-4500.2019.02.21
引用本文: 宋词, 陈婷, 吴补领. 组蛋白去乙酰化酶在口腔来源成体干细胞成骨向/成牙本向分化的研究进展[J]. 分子影像学杂志, 2019, 42(2): 234-237. doi: 10.12122/j.issn.1674-4500.2019.02.21
shu
Ci SONG, Ting CHEN, Buling WU. Progress of histone deacetylase in regulating osteogenesis/odontogenic differentiation[J]. Journal of Molecular Imaging, 2019, 42(2): 234-237. doi: 10.12122/j.issn.1674-4500.2019.02.21
Citation: Ci SONG, Ting CHEN, Buling WU. Progress of histone deacetylase in regulating osteogenesis/odontogenic differentiation[J]. Journal of Molecular Imaging, 2019, 42(2): 234-237. doi: 10.12122/j.issn.1674-4500.2019.02.21
shu

组蛋白去乙酰化酶在口腔来源成体干细胞成骨向/成牙本向分化的研究进展

doi: 10.12122/j.issn.1674-4500.2019.02.21
  • 1.

    南方医科大学 口腔医学院

  • 2.

    南方医院，广东  广州  510515

详细信息
    作者简介:

    宋词：宋 词，硕士，E-mail：905448609@qq.com

    通讯作者:

    吴补领，主任医师，教授，E-mail：wubuling1958@126.com

Progress of histone deacetylase in regulating osteogenesis/odontogenic differentiation

  • 1.

    College of Stomatology

  • 2.

    Nanfang Hospital, Southern Medical University, Guangzhou 510515, China

    摘要
  • 摘要: 基于非基因序列改变所致基因表达水平变化，如DNA甲基化和染色质构象变化等被称为表观遗传学。近年来，大量学者致力于研究表观遗传学对于多种组织中成体干细胞多向分化能力的影响，包括DNA甲基化修饰、组蛋白共价修饰、染色质重塑、基因沉默和RNA编辑等调控机制。口腔来源的成体干细胞是一类易于获得的人成体干细胞，这类细胞在组织工程学，特别是骨、牙齿再生的过程中是重要的种子细胞。研究表明，成体干细胞成骨/成牙本质向分化过程受组蛋白去乙酰化酶调控。同时，牙齿再生对于临床治疗有巨大的影响。本文阐述了组蛋白去乙酰化酶调节成骨/成牙本质向分化的研究进展以及其在牙再生医学中的应用前景。

     

    Abstract: Epigenetics is called epigenetics because of changes in gene expression level caused by non-gene sequence changes, such as DNA methylation and chromatin conformation changes. In recent years, a large number of scholars have focused on the effects of epigenetics on the multidirectional differentiation of adult stem cells in various tissues, including DNA methylation modification, histone covalent modification, chromatin remodeling, gene silencing and RNA editing. Oral-derived adult stem cells are a kind of human adult stem cells which are easy to obtain. These cells are important seed cells in tissue engineering, especially in the process of bone and tooth regeneration. Studies have shown that the osteogenic/odontogenic differentiation of adult stem cells is regulated by histone deacetylase. At the same time, tooth regeneration has a tremendous impact on clinical treatment. This paper reviews the progress of histone deacetylase in regulating osteogenesis/odontogenic differentiation and its application in dental regeneration medicine.

     

    • HTML全文
    • 参考文献(38)
  • [1] Cao DF, Yang N. Structure and catalytic mechanisms of histone deacetylases[J]. 生物化学与生物物理进展, 2015, 42(11): 978-93.
    [2] Li X, Wang Y, Hu J. Progress on epigenetic research of liver cancer[J]. 现代肿瘤医学, 2016, 9(49): 1672-9.
    [3] 李晓东, 王运帷, 胡 静. 肝癌的表观遗传学研究进展[J]. 现代肿瘤医学, 2016, 24(9): 1501-4. doi: 10.3969/j.issn.1672-4992.2016.09.049
    [4] Tu M, Li Y, Dai X. Research progress on the association between DNA methylation and oral squamous cell carcinoma[J]. 国际口腔医学杂志, 2016, 43(1): 85-90.
    [5] 陈 青, 代 智, 周 俭. 表观遗传异常在肿瘤发生发展中的研究进展[J]. 上海医药, 2015, (16): 9-13.
    [6] Bradley EW, Carpio LR, van Wijnen AJ, et al. Histone deacetylases in bone development and skeletal disorders[J]. Physiol Rev, 2015, 95(4): 1359-81. doi: 10.1152/physrev.00004.2015
    [7] Duncan HF, Smith AJ, Fleming G, et al. Epigenetic modulation of dental pulp stem cells: implications for regenerative endodontics[J]. Int Endod J, 2016, 49(5): 431-46. doi: 10.1111/iej.2016.49.issue-5
    [8] Taunton J, Hassig CA, Schreiber SL. A mammalian histone deacetylase related to the yeast transcriptional regulator Rpd3p[J]. Science, 1996, 272(5260): 408-11. doi: 10.1126/science.272.5260.408
    [9] Huynh NC, Everts V, Pavasant P. Inhibition of histone deacetylases enhances the osteogenic differentiation of human periodontal ligament cells[J]. J Cell Biochem, 2016, 117(6): 1384-95. doi: 10.1002/jcb.v117.6
    [10] Gregoretti IV, Lee YM, Goodson HV. Molecular evolution of the histone deacetylase family: functional implications of phylogenetic analysis[J]. J Mol Biol, 2004, 338(1): 17-31. doi: 10.1016/j.jmb.2004.02.006
    [11] Blander G, Guarente L. The sir2 family of protein deacetylases[J]. Annu Rev Biochem, 2004, 73(5): 417-35.
    [12] Schroeder TM, Kahler RA, Li X, et al. Histone deacetylase 3 interacts with runx2 to repress the osteocalcin promoter and regulate osteoblast differentiation[J]. J Biol Chem, 2004, 279(40): 41998-2015. doi: 10.1074/jbc.M403702200
    [13] Lu JL, Qu S, Yao B, et al. Osterix acetylation at K307 and K312 enhances its transcriptional activity and is required for osteoblast differentiation[J]. Oncotarget, 2016, 7(25): 37471-86.
    [14] Lee HW, Suh JH, Kim AY, et al. Histone deacetylase 1-mediated histone modification regulates osteoblast differentiation[J]. Molecul Endocrinol, 2006, 20(10): 2432-43. doi: 10.1210/me.2006-0061
    [15] Zhang ZL, Deepak V, Meng LY, et al. Analysis of HDAC1-mediated regulation of Runx2-induced osteopontin gene expression in C3h10t1/2 cells[J]. Biotechnol Lett, 2012, 34(2): 197-203. doi: 10.1007/s10529-011-0756-8
    [16] Liu T, Hou LC, Zhao YH, et al. Epigenetic silencing of HDAC1 by miR-449a upregulates Runx2 and promotes osteoblast differentiation[J]. Int J Mol Med, 2015, 35(1): 238-46. doi: 10.3892/ijmm.2014.2004
    [17] Kushwaha P, Khedgikar V, Sharma D, et al. MicroRNA 874-3p exerts skeletal anabolic effects epigenetically during weaning by suppressing Hdac1 expression[J]. J Biol Chem, 2016, 291(8): 3959-66. doi: 10.1074/jbc.M115.687152
    [18] Adamik J, Jin S, Sun Q, et al. EZH2 or HDAC1 inhibition reverses multiple Myeloma-Induced epigenetic suppression of osteoblast differentiation[J]. Molec Cancer Res Mcrmolcan, 2016, 15(4): 242-53.
    [19] Paino F, La Noce M, Tirino V, et al. Histone deacetylase inhibition with valproic acid downregulates osteocalcin gene expression in human dental pulp stem cells and osteoblasts: evidence for HDAC2 involvement[J]. Stem Cells, 2014, 32(1): 279-89. doi: 10.1002/stem.v32.1
    [20] Fu Y, Zhang P, Ge J, et al. Histone deacetylase 8 suppresses osteogenic differentiation of bone marrow stromal cells by inhibiting histone H3K9 acetylation and RUNX2 activity[J]. Intern J Biochem Cell Biol, 2014, 54(8): 68-77.
    [21] Jeon EJ, Lee KY, Choi NS, et al. Bone morphogenetic protein-2 stimulates Runx2 acetylation[J]. J Biol Chem, 2006, 281(24): 16502-11. doi: 10.1074/jbc.M512494200
    [22] Li H, Xie H, Liu W, et al. A novel microRNA targeting HDAC5 regulates osteoblast differentiation in mice and contributes to primary osteoporosis in humans[J]. J Clin Invest, 2009, 119(12): 3666-77. doi: 10.1172/JCI39832
    [23] Makinistoglu MP, Karsenty G. The class II histone deacetylase HDAC4 regulates cognitive, metabolic and endocrine functions through its expression in osteoblasts[J]. Mol Metab, 2015, 4(1): 64-9. doi: 10.1016/j.molmet.2014.10.004
    [24] Wein MN, Spatz J, Nishimori S, et al. HDAC5 controls MEF2C-driven sclerostin expression in osteocytes[J]. J Bone Mineral Res, 2015, 30(3): 400-11. doi: 10.1002/jbmr.2381
    [25] Westendorf JJ, Zaidi SK, Cascino JE, et al. Runx2(Cbfa1, AML-3) interacts with histone deacetylase 6 and represses the p21(CIP1/WAF1) promoter[J]. Mol Cell Biol, 2002, 22(12): 7982-92.
    [26] Jensen ED, Schroeder TM, Bailey JA, et al. Histone deacetylase 7 associates with Runx2 and represses its activity during osteoblast maturation in a deacetylation-independent manner[J]. J Bone Mineral Res, 2008, 23(3): 361-72.
    [27] Backesjo CM, Li Y, Lindgren U, et al. Activation of Sirt1 decreases adipocyte formation during osteoblast differentiation of mesenchymal stem cells[J]. J Bone Mineral Res, 2006, 21(7): 993-1002. doi: 10.1359/jbmr.060415
    [28] Lee YM, Shin SI, Shin KS, et al. The role of sirtuin 1 in osteoblastic differentiation in human periodontal ligament cells[J]. J Periodontal Res, 2011, 46(6): 712-21. doi: 10.1111/jre.2011.46.issue-6
    [29] Srivastava S, Bedi U, Roy P. Synergistic actions of insulin-sensitive and Sirt1-mediated pathways in the differentiation of mouse embryonic stem cells to osteoblast[J]. Mol Cell Endocrinol, 2012, 361(1/2): 153-64.
    [30] Xu Y, Wang SL, Tang CL, et al. Upregulation of long non-coding RNA HIF 1 alpha-anti-sense 1 induced by transforming growth factor-beta-mediated targeting of sirtuin 1 promotes osteoblastic differentiation of human bone marrow stromal cells[J]. Mol Med Rep, 2015, 12(5, B): 7233-8. doi: 10.3892/mmr.2015.4415
    [31] Duncan HF, Smith AJ, Fleming GJ. Histone deacetylase inhibitors induced differentiation and accelerated mineralization of pulp-derived cells[J]. J Endod, 2012, 38(3): 339-45. doi: 10.1016/j.joen.2011.12.014
    [32] Kang JS, Alliston T, Delston R, et al. Repression of Runx2 function by TGF-beta through recruitment of class II histone deacetylases by Smad3[J]. EMBO J, 2005, 24(14): 2543-55. doi: 10.1038/sj.emboj.7600729
    [33] Schroeder TM, Westendorf JJ. Histone deacetylase inhibitors promote osteoblast maturation[J]. J Bone Mineral Res, 2005, 20(12): 2254-63. doi: 10.1359/JBMR.050813
    [34] Hu N, Wang C, Liang X, et al. Inhibition of histone deacetylases potentiates BMP9-induced osteogenic signaling in mouse mesenchymal stem cells[J]. Cell Physiol Biochem, 2013, 32(2): 486-98. doi: 10.1159/000354453
    [35] Jin H, Park JY, Choi H, et al. HDAC inhibitor trichostatin A promotes proliferation and odontoblast differentiation of human dental pulp stem cells[J]. Tissue Eng Part A, 2013, 19(5/6): 613-24.
    [36] Zang HL, Kim HJ, Ryoo HM. A novel osteogenic activity of suberoylanilide hydroxamic acid is synergized by BMP-2[J]. J Bone Metabol, 2015, 22(2): 51-9. doi: 10.11005/jbm.2015.22.2.51
    [37] Duncan HF, Smith AJ, Fleming GJ, et al. The Histone-Deacetylase-Inhibitor suberoylanilide hydroxamic acid promotes dental pulp repair mechanisms through modulation of matrix metalloproteinase-13 activity[J]. J Cell Physiol, 2016, 231(4): 798-816. doi: 10.1002/jcp.25128
    [38] Hatakeyama Y, Hatakeyama J, Takahashi A, et al. The effect of valproic acid on mesenchymal pluripotent cell proliferation and differentiation in extracellular matrices[J]. Drug Target Insights, 2011, 25(5): 1-9.
    • 相关文章
    • 施引文献
  • 资源附件(0)
  • 加载中
WeChat 点击查看大图
计量
  • 文章访问数:  1450
  • HTML全文浏览量:  676
  • PDF下载量:  10
  • 被引次数: 0
出版历程
  • 收稿日期:  2019-02-21
  • 刊出日期:  2019-04-01

目录

    /

    返回文章
    返回
    • 版权所有© 2013《分子影像学杂志》编辑部 ICP备00000000号
    • 重点提示: Adobe Reader6可能造成全文显示不正常，请升级为Adobe Reader7或更高。
    • 地址: 广东省广州市广州大道北1838号 Tel: 020-61648176 E-mail: 

    本系统由 北京仁和汇智信息技术有限公司 开发  技术支持：info@rhhz.net

    x 关闭 永久关闭

    关于《分子影像学杂志》变更刊期通知

    各位专家、作者、读者：

    为了缩短出版时滞，促进科研成果的快速传播，我刊自2024年1月起，刊期由双月刊变更为月刊。本刊主要栏目有：基础研究、临床研究、技术方法、综述等。

    感谢各位专家、作者、读者长期以来对我刊的支持与厚爱！

    南方医科大学学报编辑部

    《分子影像学杂志》

    2023年12月27日