Gene expression profiling of Cx3cl1 in bone marrow mesenchymal stem cells by osteogenic induction.
Gene expression profiling of Cx3cl1 in bone marrow mesenchymal stem cells by osteogenic induction.
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DOI：
10.1089/omi.2009.0018
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发表时间：
2009-08
期刊：
影响因子：
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通讯作者：
Jingang Xiao;Hai Dong;Yao Wu;W. Tian;Lei Liu
中科院分区：
文献类型：
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作者：
Jingang Xiao;Hai Dong;Yao Wu;W. Tian;Lei Liu
Cx 3cl 1又称fractalkine，位于19 p12，编码趋化因子配体1（C-X3-C基序）蛋白。这种蛋白质含有393个氨基酸，是趋化因子CX 3C亚家族的唯一成员。CX 3CR 1是Cx 3cl 1的特异性受体，该配体与其受体的结合参与多种生理和病理过程。通过采用微阵列技术，我们首次证明了Cx 3cl 1在成骨诱导的大鼠骨髓间充质干细胞（BMSCs）中上调。采用实时定量聚合酶链反应（real-time PCR）检测成骨诱导后不同时间大鼠BMSCs中Cx 3cl 1基因的表达谱。结果显示，成骨诱导后大鼠BMSCs中Cx 3cl 1的表达持续增加，21 d达高峰，Cx 3cl 1可能与BMSCs的成骨分化有关。基于生物信息学分析，我们推测Cx 3cl 1可能通过调节细胞分布和聚集，促进细胞相互诱导和旁分泌而有利于骨形成微环境的形成。Cx 3cl 1还可能通过激活p38丝裂原活化蛋白激酶（MAPK）增加Runx 2转录而参与BMSCs的成骨分化和骨形成。
Cx3cl1, also called fractalkine, is located at 19p12, and encodes the chemokine (C-X3-C motif) ligand 1 protein. This protein contains 393 amino acids, and is the only member of the chemokine CX3C subfamily. CX3CR1 is the specific receptor of Cx3cl1, and the binding of this ligand and its receptor participates in a variety of physiological and pathological processes. Through employing microarray technology we demonstrated for the first time that Cx3cl1 was upregulated in osteogenic-induced rat bone marrow mesenchymal stem cells (BMSCs). To analyze the gene expression profiling of Cx3cl1 in osteogenic-induced rat BMSCs at different times, real-time quantitative polymerase chain reaction (real-time PCR) was used to assay Cx3cl1 mRNA. The results showed that the expression of Cx3cl1 in osteogenic-induced rat BMSCs increased consistently for 28 days with a peak at day 21, and Cx3cl1 may be correlated with osteogenic differentiation of BMSCs. Based on bioinformatic analyses, we hypothesize that Cx3cl1 may be beneficial to the formation of the osteoplastic microenvironment by regulating cellular distribution and aggregation, and by promoting cellular mutual induction and paracrine. Cx3cl1 may also be involved in osteogenic differentiation and bone formation of BMSCs through an increase in Runx2 transcription by activating p38 mitogen-activated protein kinase (MAPK).