Effects of leukemia inhibitory factor on proliferation and odontoblastic differentiation of human dental pulp cells.
Effects of leukemia inhibitory factor on proliferation and odontoblastic differentiation of human dental pulp cells.
复制标题
白血病抑制因子对人牙髓细胞增殖和成牙本质细胞分化的影响。
DOI：
10.1016/j.joen.2011.02.031
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发表时间：
2011-06
影响因子：
4.2
通讯作者：
王贻宁
中科院分区：
文献类型：
--
作者：
王贻宁
引言本研究的目的是确定白血病抑制因子（leukemia inhibitory factor，LIF）是否在人牙组织中表达，并对牙髓细胞（dental pulp cells，DPC）的增殖和成牙本质细胞分化产生影响。方法采用免疫组织化学方法检测白血病抑制因子（leukemia inhibitory factor，LIF）和白血病抑制因子受体（leukemia inhibitory Factor receptor，LIFR）在人牙髓中的表达。通过在不同剂量的LIF或LIF的中和抗体存在下培养人原代DPC来检查DPC的增殖。Western blot检测在LIF和/或Jak 2特异性抑制剂AG 490存在或不存在下Janus激酶2（Jak 2）和信号转导和转录激活因子3（Stat 3）的磷酸化。通过碱性磷酸酶（ALP）活性测定、骨唾液酸蛋白（BSP）和牙本质唾液酸磷蛋白（DSPP）基因表达定量和矿化结节形成等方法检测牙本质细胞向成牙本质细胞分化的情况。LIF诱导DPC增殖，可被LIF中和抗体和AG 490抑制. LIF诱导Jak 2和Stat 3的磷酸化，但在AG 490存在下不诱导。在矿化诱导培养基存在或不存在的情况下，DPC的ALP活性被LIF抑制。LIF还能抑制矿化结节的形成和BSP、DSPP的表达。结论LIF和LIFR在人牙髓中均有表达。LIF促进牙源性前体细胞增殖，通过Jak 2-Stat 3信号通路抑制牙源性前体细胞向成牙本质细胞分化。
INTRODUCTIONThe purpose of this study was to determine whether the leukemia inhibitory factor (LIF) is expressed in human dental tissue and exerts its effect on proliferation and odontoblastic differentiation of the dental pulp cells (DPCs).METHODSAn immunohistochemical assay was used to detect the expression of LIF and leukemia inhibitory factor receptor (LIFR) in the human dental pulp. The proliferation of DPCs was examined by culturing human primary DPCs in the presence of LIF with different doses or the neutralizing antibody to LIF. Western blot was performed to assay the phosphorylation of Janus kinase 2 (Jak2) and signal transducer and activator of transcription 3 (Stat3) in the presence or absence of LIF and/or AG 490, a specific inhibitor of Jak2. The odontoblastic differentiation of DPCs was determined using the alkaline phosphatase (ALP) activity assay, quantification of bone sialoprotein (BSP) and dentin sialophosphoprotein (DSPP) gene expression, and mineralization nodule formation.RESULTSLIF and LIFR were present in the odontoblasts and DPCs. LIF induced proliferation of DPCs, which was inhibited by the LIF neutralizing antibody and AG 490. LIF induced phosphorylation of Jak2 and Stat3 but not in the presence of the AG490. ALP activity of DPCs, in the absence or presence of mineralization induction medium, was inhibited by LIF. Furthermore, the mineralization nodule formation and the expression of BSP and DSPP were inhibited by LIF. This inhibition on differentiation was attenuated by the AG490.CONCLUSIONLIF and LIFR are expressed in the human dental pulp. LIF promotes the proliferation of DPCs, and the odontoblastic differentiation is inhibited via the Jak2-Stat3 signaling pathway.
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影响因子：
3.1
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通讯作者：
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