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在PerioGlas上培养的成骨样细胞的基因图谱

Genetic portrait of osteoblast-like cells cultured on PerioGlas.

作者信息

Carinci Francesco, Palmieri Annalisa, Martinelli Marcella, Perrotti Vittoria, Piattelli Adriano, Brunelli Giorgio, Arlotti Marzia, Pezzetti Furio

机构信息

Department of Embryology and Morphology, University of Ferrara.

出版信息

J Oral Implantol. 2007;33(6):327-33. doi: 10.1563/1548-1336(2007)33[327:GPOOCC]2.0.CO;2.

Abstract

PerioGlas (PG) is an alloplastic material used for grafting periodontal osseous defects since 1995. In animal models it has been histologically proven that PG achieves good repair of surgically created defects. In clinical trials, PG has been shown to be effective as an adjunct to conventional surgery in treating intrabony defects. Because the molecular events by which PG is able to alter osteoblast activity to promote bone formation are poorly understood, we investigated genes that are differently regulated in osteoblast-like cells exposed to PG. Bone formation can be attributable to ostegenesis (ie, direct stimulation of osteoblast to produce new bone), osteoconduction (which operates like a scaffold), or both processes. By using DNA microarrays containing 20 000 oligonucleotides, we identified several genes in which expression was significantly downregulated in a MG63 cell line cultured with PerioGlas (US Biomaterials Corp, Alachua, Fla). Specifically, PG is able to downregulate some functional activities of osteoblast-like cells: it acts on signal transduction, especially on the transforming growth factor beta (TGFB) paracrine network; it inhibits apoptosis; it decreases cell adhesion with consequent enhancement of cell mobility and migration; and it acts on bone marrow stem cells (ie, CD34). In conclusion, PG acts on bone formation by determining both osteoconduction (as demonstrated by the reduced cell adhesion) and ostegenesis (as shown by TGFB-related proteins and stem cell markers).

摘要

自1995年以来,牙周玻璃(PG)一直是一种用于移植牙周骨缺损的异质材料。在动物模型中,组织学已证实PG能很好地修复手术造成的缺损。在临床试验中,PG已被证明作为传统手术的辅助手段治疗骨内缺损是有效的。由于PG能够改变成骨细胞活性以促进骨形成的分子机制尚不清楚,我们研究了在暴露于PG的成骨样细胞中差异调节的基因。骨形成可归因于成骨作用(即直接刺激成骨细胞产生新骨)、骨传导作用(其作用类似于支架)或这两个过程。通过使用含有20000个寡核苷酸的DNA微阵列,我们在与牙周玻璃(美国生物材料公司,佛罗里达州阿拉楚阿)一起培养的MG63细胞系中鉴定出几个表达显著下调的基因。具体而言,PG能够下调成骨样细胞的一些功能活性:它作用于信号转导,特别是转化生长因子β(TGFB)旁分泌网络;它抑制细胞凋亡;它减少细胞粘附,从而增强细胞的移动性和迁移能力;并且它作用于骨髓干细胞(即CD34)。总之,PG通过决定骨传导作用(如细胞粘附减少所示)和成骨作用(如TGFB相关蛋白和干细胞标志物所示)来影响骨形成。

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