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| Effect of Basic Fibroblast Growth Factor 2 on Differentiation of Rat Adipose Derived Stem Cells into Odontoblast Like Cells and its Mechanism |
| HE Hui-ping, JI Xiao-ting |
| Department of Stomatology,Ninth Hospital of Xi'an,Xi'an Shaanxi 710054 |
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Abstract 【Objective】Objective to investigate the effect of basic fibroblast growth factor-2 (FGF-2) on the differentiation of rat adipose derived stem cells (ADSCs) into odontoblast like cells and its mechanism. 【Methods】 ADSCs were isolated and identified from bilateral inguinal adipose tissue of rats. The third generation ADSCs were randomly divided into blank control group (NG group),negative control group (siRNA-NC group),FGF-2 silencing group (TGF-2-siRNA group) and pathway activator group. The expression level of FGF-2 in ADSCs was detected by real-time fluorescent quantitative PCR; The proliferation of ADSCs in each group was detected by CCK-8 method; Alizarin red staining was used to observe the odontogenic differentiation of ADSCs in each group; Western blotting and enzyme-linked immunosorbent assay (ELISA) were used to detect neuropilin 1 (NRP1),dentin sialoprotein (DSPP),dentin matrix protein 1 (DMP1) and wingless MMTV integration site family members/β-catenin (Wnt/β-catenin) pathway protein level. 【Results】ADSCs were successfully isolated and identified;Compared with the NG group and the siRNA NC group; the expression levels of FGF-2 mRNA,NRP1,DSPP,DMP1,Wnt and β-catenin protein of the ADSCs in the FGF-2-siRNA group and the pathway activator group decreased (P<0.05),the proliferation inhibition rate of ADSCs increased (P<0.05); Compared with the FGF-2-siRNA group,the expression of FGF-2 mRNA,NRP1,DSPP,DMP1,β-catenin protein and Wnt increased (P<0.05); the proliferation inhibition rate of ADSCs decreased (P<0.05).【Conclusion】 FGF-2 can affect Wnt/β-catenin activation pathway . This may be related to the proliferation of rat ADSCs and their differentiation into odontoblast like cells,which may provide a new idea for the treatment of tooth defects.
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Received: 07 February 2022
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2022, Vol. 39 
