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首页> 外文期刊>Journal of pharmacological sciences. >Current topics in pharmacological research on bone metabolism: Promyelotic leukemia zinc finger (PLZF) and tumor necrosis factor-alpha-stimulated gene 6 (TSG-6) identified by gene expression analysis play roles in the pathogenesis of ossification of
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Current topics in pharmacological research on bone metabolism: Promyelotic leukemia zinc finger (PLZF) and tumor necrosis factor-alpha-stimulated gene 6 (TSG-6) identified by gene expression analysis play roles in the pathogenesis of ossification of

机译：骨代谢药理学研究的当前主题：通过基因表达分析鉴定的早幼粒细胞白血病锌指（PLZF）和肿瘤坏死因子-α刺激基因6（TSG-6）在骨化的发病机理中起作用

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To understand the molecular pathogenesis of ossification of the posterior longitudinal ligament of the spine (OPLL), an ectopic bone formation disease, we performed cDNA microarray analysis on cultured ligament cells from OPLL patients to understand the molecular pathogenesis of OPLL. We identified promyelotic leukemia zinc finger (PLZF) as one of up-regulated genes and tumor necrosis factor-alpha-stimulated gene 6 (TSG-6) as one of down-regulated gene during osteoblastic differentiation. We investigated the roles of PLZF in the regulation of osteoblastic differentiation of human mesenchymal stem cells (hMSCs) and C2C12 cells. siRNA-mediated gene-silencing of PLZF resulted in a reduction of the expression of osteoblast-specific genes such as the alkaline phosphatase, collagen 1A1, Runx2/CBFA1, and osteocalcin genes in the presence of osteogenic differentiation medium (OS) in hMSCs. The overexpression of PLZF induced CBFA1 induction, suggesting that PLZF is an upstream regulator of CBFA1 and thereby participates in promoting the ossification of spinal ligament cells in OPLL patients. Adenovirus-mediated TSG-6 overexpression in hMSCs resulted in suppression of osteoblastic differentiation induced by either BMP-2 or OS. TSG-6 can bind to BMP-2 directly and thereby could inhibit BMP-2 signaling. Taken together, these findings indicate that PLZF and TSG-6 play important roles in early osteoblastic differentiation.
机译：为了了解脊柱后纵韧带（OPLL）的骨化的分子发病机制（一种异位骨形成疾病），我们对来自OPLL患者的培养的韧带细胞进行了cDNA微阵列分析，以了解OPLL的分子发病机制。我们鉴定了成骨细胞分化过程中早幼粒细胞白血病锌指（PLZF）为上调基因之一，肿瘤坏死因子α刺激基因6（TSG-6）为下调基因之一。我们研究了PLZF在调节人间充质干细胞（hMSCs）和C2C12细胞成骨细胞分化中的作用。在hMSC中存在成骨分化培养基（OS）的情况下，siRNA介导的PLZF基因沉默导致成骨细胞特异性基因（如碱性磷酸酶，胶原1A1，Runx2 / CBFA1和骨钙素基因）的表达减少。 PLZF的过表达诱导了CBFA1的诱导，这表明PLZF是CBFA1的上游调节剂，因此参与了促进OPLL患者脊椎韧带细胞骨化的过程。腺病毒介导的hMSC中TSG-6的过度表达可抑制BMP-2或OS诱导的成骨细胞分化。 TSG-6可以直接与BMP-2结合，从而可以抑制BMP-2信号传导。综上所述，这些发现表明PLZF和TSG-6在早期成骨细胞分化中起重要作用。

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