Transforming growth factor-β1 promotes early odontoblastic differentiation of dental pulp stem cells via activating AKT, Erk1/2 and p38 MAPK pathways.
Transforming growth factor-β1 promotes early odontoblastic differentiation of dental pulp stem cells via activating AKT, Erk1/2 and p38 MAPK pathways.
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DOI：
10.1016/j.jds.2022.06.027
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发表时间：
2023-01
影响因子：
3.5
通讯作者：
Yu, Qing
中科院分区：
文献类型：
--
作者：
Bai, Yu;Cheng, Xiaogang;Liu, Xin;Guo, Qian;Wang, Zhihua;Fu, Yi;He, Wenxi;Yu, Qing
转化生长因子β1在牙髓-牙本质复合体的再生和修复中起重要作用。然而，转化生长因子-β1在成牙本质细胞分化中的生物学作用尚不清楚，主要是由于其分化过程受复杂的信号通路调控。本研究旨在探讨转化生长因子-β-1调控牙髓干细胞早期分化的信号通路及其功能作用。用1 ng/mL转化生长因子-β-1处理DPSCs，Western blotting检测蛋白激酶B(AKT)、小鼠母亲抗十碳瘫痪3(SMAD3)、p38MAPK、c-jun氨基末端激酶和细胞外信号调节激酶1/2(ERK1/2)的活性。将DPSC暴露于含有转化生长因子-β1的矿化培养液中，通过检测碱性磷酸酶、1型胶原α1、牙本质基质蛋白1和矮小相关转录因子2的表达来评价早期牙源性分化。转化生长因子-β-1在12 0min内可刺激DPSCAKT、Smad3、p38MAPK、ERK1/2和JNK1的磷酸化。转化生长因子-DMP-1促进碱性磷酸酶活性及COL1a、β-1和Runx2水平升高。LY294002、U0126和SB203580可减弱转化生长因子-β-1对DPSCs的作用，而SIS3和SP600125组无明显作用。转化生长因子β-1通过激活AKT、ERK1/2和p38MAPK信号通路促进DPSCs向成牙本质细胞分化的早期，而不是通过Smad3和JNK3途径。
TGF-β1 (Transforming growth factor-β1) plays an important role in the regeneration and repair of pulp-dentin complex. However, the biological function of TGF-β1 on odontoblastic differentiation remains unclear, mainly due to the processes of differentiation were controlled by complex signaling pathways. This study aimed to investigate the signaling pathways involved in regulating the early differentiation of dental pulp stem cells (DPSCs) by TGF-β1 and their functional role. DPSCs were treated with 1 ng/mL TGF-β1 and Western blotting was conducted to examine the activation of protein kinase B (AKT), small mothers against decapentaplegic 3 (Smad3), p38 mitogen-activated protein kinase (p38 MAPK), c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase 1/2 (Erk1/2). DPSCs were exposed to mineralization medium contained TGF-β1 with/without the specific signaling pathway inhibitors, and early odontogenic differentiation was evaluated by assessing the expression of alkaline phosphatase (ALP), collagen type 1 alpha 1 (COL1A), dentin matrix protein 1 (DMP-1) and runt-related transcription factor 2 (Runx2). TGF-β1 stimulated AKT, Smad3, p38 MAPK, Erk1/2 and JNK phosphorylation in DPSCs within 120 min. TGF-β1 enhanced ALP activity and elevated levels of COL1A, DMP-1 and Runx2. LY294002, U0126 and SB203580 attenuated the effect of TGF-β1 on DPSCs, however, the SIS3 and SP600125 treated groups had no significant effect. TGF-β1 promotes the early stage of odontoblastic differentiation in DPSCs by activating AKT, Erk1/2 and p38 MAPK signaling pathways, but not by Smad3 and JNK.
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影响因子：
2.9
作者：
Qin, Wei;Liu, Pengcheng;Lin, Zhengmei
通讯作者：
Lin, Zhengmei
影响因子：
2.5
作者：
GONÇALVES, Lidiany Freitas;FERNANDES, Ana Paula;SAKAI, Vivien Thiemy
通讯作者：
SAKAI, Vivien Thiemy
影响因子：
2.5
作者：
Eren, Selen Kucukkaya;Zirh, Elham Bahador;Parashos, Peter
通讯作者：
Parashos, Peter
影响因子：
7.2
作者：
Grafe I;Alexander S;Peterson JR;Snider TN;Levi B;Lee B;Mishina Y
通讯作者：
Mishina Y
TGFβ 信号的背景
DOI：
10.1038/nrm3434
发表时间：
2012-10
期刊：
Nature reviews. Molecular cell biology
影响因子：
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作者：
通讯作者：
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