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首页> 外文期刊>International journal of molecular medicine >FGF-2 induces the proliferation of human periodontal ligament cells and modulates their osteoblastic phenotype by affecting Runx2 expression in the presence and absence of osteogenic inducers
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FGF-2 induces the proliferation of human periodontal ligament cells and modulates their osteoblastic phenotype by affecting Runx2 expression in the presence and absence of osteogenic inducers

机译:FGF-2通过在存在和不存在成骨诱导剂的情况下影响Runx2表达来诱导人牙周膜细胞增殖并调节其成骨细胞表型

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The exact phenotype of human periodontal ligament cells?(hPDLCs) remains a controversial area. Basic fibroblast growth factor?(FGF?2) exhibits various functions and its effect on hPDLCs is also controversial. Therefore, the present study examined the effect of FGF?2 on the growth and osteoblastic phenotype of hPDLCs with or without osteogenic inducers (dexamethasone and β?glycerophosphate). FGF?2 was added to defined growth culture medium and osteogenic inductive culture medium. Cell proliferation, osteogenic differentiation and mineralization were measured. The selected differentiation markers, Runx2, collagen type?Ⅰ, α1?(Col1a1), osteocalcin?(OCN) and epidermal growth factor receptor?(EGFR), were investigated by reverse transcription?quantitative polymerase chain reaction?(RT?qPCR). Runx2 and OCN protein expression was measured by western blotting. FGF?2 significantly increased the proliferation of hPDLCs, but did not affect alkaline phosphatase activity. RT?qPCR analysis revealed enhanced mRNA expression of Runx2, OCN and EGFR, but suppressed Col1a1 gene expression in the absence of osteogenic inducers, whereas all these gene levels had no clear trend in their presence. The Runx2 protein expression was clearly increased, but the OCN protein level showed no evident trend. The mineralization assay demonstrated that FGF?2 inhibited mineralized matrix deposition with osteogenic inducers. These results suggested that FGF?2 induces the growth of immature hPDLCs, which is a competitive inhibitor of epithelial downgrowth, and suppresses their differentiation into mineralized tissue by affecting Runx2 expression. Therefore, this may lead to the acceleration of periodontal regeneration.
机译:人类牙周膜细胞的确切表型仍是一个有争议的领域。碱性成纤维细胞生长因子β(FGFβ2)具有多种功能,其对hPDLC的作用也存在争议。因此,本研究研究了FGFβ2对有或没有成骨诱导剂(地塞米松和β-甘油磷酸酯)的hPDLCs生长和成骨细胞表型的影响。将FGF 2加入到确定的生长培养基和成骨诱导培养基中。测量细胞增殖,成骨分化和矿化。通过逆转录-定量聚合酶链反应(RT-qPCR)研究了所选择的分化标志物Runx2,胶原类型Ⅰ,α1α(Col1a1),骨钙蛋白(OCN)和表皮生长因子受体(EGFR)。 Runx2和OCN蛋白表达通过蛋白质印迹法测量。 FGF 2显着增加hPDLC的增殖,但不影响碱性磷酸酶的活性。 RT?qPCR分析显示Runx2,OCN和EGFR的mRNA表达增强,但是在没有成骨诱导剂的情况下抑制了Col1a1基因表达,而所有这些基因水平在它们存在时均没有明确的趋势。 Runx2蛋白表达明显增加,但OCN蛋白水平未显示明显趋势。矿化试验表明,FGFβ2通过成骨诱导剂抑制了矿化基质的沉积。这些结果表明,FGFβ2诱导不成熟的hPDLC的生长,该hPDLC是上皮下生长的竞争性抑制剂,并通过影响Runx2的表达抑制其分化为矿化组织。因此,这可能导致牙周再生的加速。

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