Stromal cell-derived factor 1 protects human periodontal ligament stem cells against hydrogen peroxide-induced apoptosis
Stromal cell-derived factor 1 protects human periodontal ligament stem cells against hydrogen peroxide-induced apoptosis
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DOI：
10.3892/mmr.2017.7192
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发表时间：
2017-10-01
影响因子：
3.4
通讯作者：
Fu, Baiping
中科院分区：
文献类型：
--
作者：
Feng, Yimiao;Fu, Xiaohui;Fu, Baiping
牙周膜干细胞(PDLSCs)被认为是一种很有前途的牙科组织再生细胞来源。基质细胞衍生因子1[SDF-1，也称为趋化因子(C-X-C基序)配体12]被认为是参与组织再生过程中干/祖细胞趋化和归巢的关键细胞因子。本研究描述了SDF-1在保护PDLSCs免受氧化应激诱导的细胞凋亡中的先前未被怀疑的作用。在本研究中，PDLSCs暴露于不同浓度的H_2O_2中12h，诱导细胞凋亡，然后检测细胞存活率，并检测caspase-3和-9的表达水平。为了探讨这种保护作用的可能机制，我们检测了丝裂原活化蛋白激酶(MAPK)信号通路的关键蛋白--总的和磷酸化的细胞外信号调节激酶(ERK)的蛋白表达水平。本研究的结果表明，SDF-1预处理提高了过氧化氢处理后的细胞存活率，并下调了活化的caspase-3和-9的蛋白表达水平。此外，SDF-1处理增加了ERK的磷酸化。SDF-1的保护作用可被MAPK/ERK抑制剂PD98059部分抑制，从而降低细胞存活率。本研究结果提示，SDF-1治疗是一种潜在的提高PDLSCs存活率的策略，可能有利于牙齿组织的再生。
Periodontal ligament stem cells (PDLSCs) are considered a promising cell source for dental tissue regeneration. Stromal cell-derived factor 1 [SDF-1, also known as chemokine (C-X-C motif) ligand 12] is regarded as a critical cytokine involved in stem/progenitor cell chemotaxis and homing during tissue regeneration. The present study described a previously unsuspected role for SDF-1 in the protection of PDLSCs against oxidative stress-induced apoptosis. In the present study, apoptosis was induced by exposure of PDLSCs to various concentrations of H2O2 for 12 h, following which cell viability was assessed, and cleaved caspase-3 and -9 expression levels were evaluated. To investigate the potential mechanism underlying this protection, the protein expression levels of total and phosphorylated extracellular signal-regulated kinase (ERK), a key protein of the mitogen-activated protein kinase (MAPK) signaling pathway, were examined. The results of the present study revealed that SDF-1 pretreatment increased cell viability following H2O2 administration, and downregulated protein expression levels of activated caspase-3 and -9. Furthermore, treatment with SDF-1 increased the phosphorylation of ERK. The protective effect of SDF-1 was partially inhibited by treatment with PD98059, a MAPK/ERK inhibitor, which decreased cell viability. The results of the present study suggested that SDF-1 treatment is a potential strategy to improve the survival of PDLSCs, which may be beneficial for dental tissue regeneration.