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Periostin plays role in force‐induced stem cell potential by periodontal ligament stem cells

机译:Periostin在牙周韧带干细胞中起在力诱导的干细胞潜力中起作用

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Abstract Mechanical stimuli have been shown to play an important role in directing stem cell fate and maintenance of tissue homeostasis. One of the functions of the mechanoresponsive tissue periodontal ligament (PDL) is to withstand the functional forces within the oral cavity. Periodontal ligament stem cells (PDLSCs) derived from periodontal tissue have been demonstrated to be able to respond directly to mechanical forces. However, the mechanisms of action of mechanical force on PDLSCs are not totally understood. The aim of this study was to investigate the mechanisms by which compressive force affects PDLSCs, especially their stemness properties. PDLSCs were established from extracted human third molars; their stem cell characteristics were validated by detecting the expression of stem cell markers and confirming their ability to differentiate into osteogenic and adipogenic lineages. PDLSCs were subjected to various magnitudes of static compressive force (0 [control], 0.5, 1.0, 1.5, or 2?g/cm 2 ). Application of 1.0?g/cm 2 compressive force significantly upregulated a panel of stem cell marker genes, including NANOG and OCT4 . Conversely, higher force magnitudes downregulated these genes. Mechanical loading also upregulated periostin, a matrix protein that plays important roles in tissue morphogenesis. Interestingly, knockdown of periostin using siRNA abolished force‐induced stem cell marker expression in PDLSCs. This study suggests a proper magnitude of compressive force could be one important factor involved in the modulation of the pluripotency of PDLSCs through the action of periostin. The precise mechanism by which periostin regulates stemness requires further detailed investigation.
机译:摘要已经显示出机械刺激在引导干细胞命运和维持组织稳态方面发挥重要作用。机械偶联组织牙周韧带(PDL)的一个功能是承受口腔内的功能力。已经证明源自牙周组织的牙周韧带干细胞(PDLSCs)能够直接响应机械力。然而,没有完全理解PDLSC上的机械力的作用机制。本研究的目的是研究压缩力影响PDLSC的机制,尤其是它们的茎性能。从提取的人的第三磨牙建立了PDLSCs;通过检测干细胞标记物的表达并确认它们分化成骨质发生和脂肪素谱系的能力来验证它们的干细胞特征。对PDLSC进行各种静态压缩力(0 [对照],0.5,1.0,1.5或2·G / cm 2)。施加1.0?G / cm 2压缩力显着上调了干细胞标志物基因的面板,包括纳米和Oct4。相反,较高的力幅度下调这些基因。机械负载也上调肝素,一种在组织形态发生中起重要作用的基质蛋白。有趣的是,使用siRNA废除力诱导的PDLSC诱导的力诱导的力诱导的干细胞标记物表达的肝蛋白敲低。本研究表明,抗压力的适当幅度可能是通过肝素的作用来调节PDLSC的多能性的一个重要因素。 Periostin调节茎干的精确机制需要进一步详细的调查。

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