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Vitamin D Promotes Odontogenic Differentiation of Human Dental Pulp Cells via ERK Activation

机译:维生素D通过ERK激活促进人牙髓细胞的牙源性分化

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摘要

The active metabolite of vitamin D such as 1α,25-dihydroxyvitamin D3 (1α,25(OH)2D3) is a well-known key regulatory factor in bone metabolism. However, little is known about the potential of vitamin D as an odontogenic inducer in human dental pulp cells (HDPCs) in vitro . The purpose of this study was to evaluate the effect of vitamin D3 metabolite, 1α,25(OH)2D3, on odontoblastic differentiation in HDPCs. HDPCs extracted from maxillary supernumerary incisors and third molars were directly cultured with 1α,25(OH)2D3 in the absence of differentiation-inducing factors. Treatment of HDPCs with 1α,25(OH)2D3 at a concentration of 10 nM or 100 nM significantly upregulated the expression of dentin sialophosphoprotein (DSPP) and dentin matrix protein1 (DMP1), the odontogenesis-related genes. Also, 1α,25(OH)2D3 enhanced the alkaline phosphatase (ALP) activity and mineralization in HDPCs. In addition, 1α,25(OH)2D3 induced activation of extracellular signal-regulated kinases (ERKs), whereas the ERK inhibitor U0126 ameliorated the upregulation of DSPP and DMP1 and reduced the mineralization enhanced by 1α,25(OH)2D3. These results demonstrated that 1α,25(OH)2D3 promoted odontoblastic differentiation of HDPCs via modulating ERK activation.
机译:1α,25-二羟基维生素D 3 (1α,25(OH) 2 D 3 )等维生素D的活性代谢产物骨代谢的关键调节因子。但是,关于维生素D作为人牙髓细胞(HDPC)体外成牙诱导剂的潜力知之甚少。这项研究的目的是评估维生素D 3 代谢产物1α,25(OH) 2 D 3 对牙本质成骨细胞分化的影响在HDPC中。从上颌上切牙和第三磨牙中提取的HDPCs在没有分化诱导因子的情况下直接与1α,25(OH) 2 D 3 培养。用浓度为10 nM或100 nM的1α,25(OH) 2 D 3 处理HDPCs显着上调了牙本质唾液磷蛋白(DSPP)和牙本质基质蛋白的表达1 (DMP1),牙源发生相关基因。此外,1α,25(OH) 2 D 3 增强了HDPC中的碱性磷酸酶(ALP)活性和矿化作用。此外,1α,25(OH) 2 D 3 诱导了细胞外信号调节激酶(ERKs)的激活,而ERK抑制剂U0126改善了DSPP和DMP1的上调并减少了1α,25(OH) 2 D 3 增强的矿化作用。这些结果表明,1α,25(OH) 2 D 3 通过调节ERK活化促进了HDPC的牙本质分化。

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