肿瘤抑制因子
细胞生物学
牙髓干细胞
骨形态发生蛋白2
间充质干细胞
细胞分化
化学
运行x2
干细胞
生物
成骨细胞
免疫学
细胞因子
白细胞介素6
体外
基因
生物化学
作者
Xiaoxing Feng,Shuling Shen,Peipei Cao,Linhe Zhu,Ye Zhang,Ke Zheng,Guoliang Feng,Dongmei Zhang
出处
期刊:Cytotechnology
[Springer Nature]
日期:2016-07-04
卷期号:68 (6): 2699-2709
被引量:15
标识
DOI:10.1007/s10616-016-9995-9
摘要
Dental pulp stem cells (DPSCs) are a type of mesenchymal stem cells, which have the self-renewal and multi-lineage differentiation potential, including chondrocytes, adipocytes, neural cells and osteoblasts. So they play a significant role in pulp repair and bone regeneration. Oncostatin M (OSM), one of the IL-6 family cytokines, inhibits adipogenic differentiation and stimulates osteogenic differentiation of human bone marrow mesenchymal stem cells. However, the effect of OSM on DPSCs is unclear. We found that OSM induced osteogenic differentiation of DPSCs, promoting matrix mineralization as measured by Alizarin Red S staining. OSM also increased expression of osteogenesis-associated gene products Alkaline phosphatase, Bone morphogenetic protein 2 (BMP2), Runt-related transcription factor 2 and Osteocalcin (OCN) as assessed by immunoblotting. We also found that OSM activated the Signal Transducer And Activator Of Transcription 3 (STAT3) pathway during the osteogenic differentiation of DPSCs. Blocking the osteogenic differentiation by silencing of STAT3 can significantly inhibit OSM-induced osteogenic differentiation of DPSCs and the expression of related genes, furthermore matrix mineralization was also suppressed. In summary, OSM promotes osteoblastic differentiation of DPSCs and osteogenesis-related genes expression through the JAK3/STAT3 signaling pathway which may be useful for the autologous transplantation of DPSCs.
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