国际口腔医学杂志 ›› 2016, Vol. 43 ›› Issue (3): 343-347.doi: 10.7518/gjkq.2016.03.020
林颖1,秦伟1,邹瑞2,林正梅1
Lin Ying1, Qin Wei1, Zou Rui2, Lin Zhengmei1
摘要: 通过诱导牙髓干细胞(DPSC)向成牙本质细胞方向分化,龋源性牙髓炎的治疗将不再局限于根管治疗这一临床选择,修复治疗也不再成为缺失牙治疗的唯一方案。促丝裂原激活蛋白激酶(MAPK),尤其是P38MAPK通过直接或间接磷酸化特定的转录因子,将细胞外刺激信号转导至细胞及其核内,从而引起一系列细胞生物学反应,如细胞增殖、分化、转化和程序性死亡。骨形态发生蛋白-2、矿物三氧化物聚合体和Biodentine皆可诱导DPSC向成牙本质细胞分化,而三者正是通过MAPK信号转导通路发挥作用的。在组织工程支架诱导DPSC分化过程中,支架材料通过激活P38MAPK信号转导通路促进了DPSC的分化。此外,MAPK信号转导通路参与牙髓损伤修复中DPSC的迁移、黏附和分化,参与牙髓损伤修复中牙本质的形成。由于MAPK信号转导通路在细胞增殖、分化和生存等过程中都起着十分关键的作用,因此,深入研究其反应分子、作用底物和作用机制有着重要的理论和临床意义。
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[1] Gronthos S, Mankani M, Brahim J, et al. Postnatal human dental pulp stem cells(DPSC) in vitro and in vivo[J]. Proc Natl Acad Sci USA, 2000, 97(25):13625-13630. [2] Gronthos S, Brahim J, Li W, et al. Stem cell properties of human dental pulp stem cells[J]. J Dent Res, 2002, 81(8):531-535. [3] Huang AH, Chen YK, Lin LM, et al. Isolation and characterization of dental pulp stem cells from a supernumerary tooth[J]. J Oral Pathol Med, 2008, 37(9):571-574. [4] Harada H, Kettunen P, Jung HS, et al. Localization of putative stem cells in dental epithelium and their association with Notch and FGF signaling[J]. J Cell Biol, 1999, 147(1):105-120. [5] Téclès O, Laurent P, Zygouritsas S, et al. Activation of human dental pulp progenitor/stem cells in response to odontoblast injury[J]. Arch Oral Biol, 2005, 50(2):103-108. [6] Shi S, Robey PG, Gronthos S. Comparison of human dental pulp and bone marrow stromal stem cells by cDNA microarray analysis[J]. Bone, 2001, 29(6):532-539. [7] Blüthgen N, Legewie S. Systems analysis of MAPK signal transduction[J]. Essays Biochem, 2008, 45:95-107. [8] Patil CS, Kirkwood KL. P38MAPK signaling in oralrelated diseases[J]. J Dent Res, 2007, 86(9):812-825. [9] Ruch JV, Lesot H, Bègue-Kirn C. Odontoblast differentiation[J]. Int J Dev Biol, 1995, 39(1):51-68. [10] Smith AJ, Cassidy N, Perry H, et al. Reactionary dentinogenesis[J]. Int J Dev Biol, 1995, 39(1):273-280. [11] Qin W, Lin ZM, Deng R, et al. P38a MAPK is involved in BMP-2-induced odontoblastic differentiation of human dental pulp cells[J]. Int Endod J, 2012, 45(3):224-233. [12] Zhao X, He W, Song Z, et al. Mineral trioxide aggregate promotes odontoblastic differentiation via mitogen-activated protein kinase pathway in human dental pulp stem cells[J]. Mol Biol Rep, 2012, 39(1):215-220. [13] Luo Z, Kohli MR, Yu Q, et al. Biodentine induces human dental pulp stem cell differentiation through mitogen-activated protein kinase and calcium-/ calmodulin-dependent protein kinaseⅡpathways[J]. J Endod, 2014, 40(7):937-942. [14] Simon SR, Berdal A, Cooper PR, et al. Dentin-pulp complex regeneration: from lab to clinic[J]. Adv Dent Res, 2011, 23(3):340-345. [15] Zhang H, Liu S, Zhou Y, et al. Natural mineralized scaffolds promote the dentinogenic potential of dental pulp stem cells via the mitogen-activated protein kinase signaling pathway[J]. Tissue Eng Part A, 2012, 18(7/8):677-691. [16] Goldberg M, Smith AJ. Cells and extracellular matrices of dentin and pulp: a biological basis for repair and tissue engenerring[J]. Crit Rev Oral Biol Med, 2004, 15(1):13-27. [17] Fitzgerald M, Chiego DJ, Heys DR. Autoradiographic analysis of odontoblast replacement following pulp exposure in primate teeth[J]. Arch Oral Biol, 1990, 35(9):707-715. [18] Sloan AJ, Smith AJ. Stem cells and the dental pulp: potential roles in dentine regeneration and repair[J]. Oral Dis, 2007, 13(2):151-157. [19] Hosoya S, Matsushima K, Ohbayashi E, et al. Stimulation of interleukin-1beta-independent interleukin-6 production in human dental pulp cells by lipopolysaccharide[J]. Biochem Mol Med, 1996, 59(2):138-143. [20] Warfvinge J. Morphometric analysis of teeth with inflamed pulp[J]. J Dent Res, 1987, 66(1):78-83. [21] Li D, Fu L, Zhang Y, et al. The effects of LPS on adhesion and migration of human dental pulp stem cells in vitro[J]. J Dent, 2014, 42(10):1327-1334. [22] He W, Wang Z, Luo Z, et al. LPS promote the odontoblastic differentiation of human dental pulp stem cells via MAPK signaling pathway[J]. J Cell Physiol, 2015, 230(3):554-561. [23] Simon S, Smith AJ, Berdal A, et al. The MAP kinase pathway is involved in odontoblast stimulation via p38 phosphorylation[J]. J Endod, 2010, 36(2):256-259. [24] Güven G, Altun C, Günhan O, et al. Co-expression of cyclooxygenase-2 and vascular endothelial growth factor in inflamed human pulp: an immunohistochemical study[J]. J Endod, 2007, 33(1):18-20. [25] Yoshida S. A scanning electron microscope study of vascular development in the dental papilla of prenatal rat molars[J]. Anat Embryol, 1991, 183(4):379-384. [26] Botero TM, Son JS, Vodopyanov D, et al. MAPK signaling is required for LPS-induced VEGF in pulp stem cells[J]. J Dent Res, 2010, 89(3):264-269. [27] Vandomme J, Touil Y, Ostyn P, et al. Insulin-like growth factor 1 receptor and p38 mitogen-activated protein kinase signals inversely regulate signal transducer and activator of transcription 3 activity to control human dental pulp stem cell quiescence, propagation, and differentiation[J]. Stem Cells Dev, 2014, 23(8):839-851. [28] Bikkavilli RK, Feigin ME, Malbon CC. p38 mitogenactivated protein kinase regulates canonical Wntbeta-catenin signaling by inactivation of GSK3beta [J]. J Cell Sci, 2008, 121(Pt 21):3598-3607. [29] Faust D, Schmitt C, Oesch F, et al. Differential p38-dependent signalling in response to cellular stress and mitogenic stimulation in fibroblasts[J]. Cell Commun Signal, 2012, 10:6. [30] Wood CD, Thornton TM, Sabio G, et al. Nuclear localization of P38MAPK in response to DNA damage [J]. Int J Biol Sci, 2009, 5(5):428-437. [31] Gong X, Ming X, Deng P, et al. Mechanisms regulating the nuclear translocation of p38 MAP kinase[J]. J Cell Biochem, 2010, 110(6):1420-1429. [32] Ruch JV. Odontoblast commitment and differentiation[J]. Biochem Cell Biol, 1998, 76(6):923-938. (本文采编 王晴) |
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