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Natural variation in four human collagen genes across an ethnically diverse population.四个人类胶原蛋白基因在不同种族人群中的自然变异。
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The performance of human dental pulp stem cells on different three-dimensional scaffold materials.人牙髓干细胞在不同三维支架材料上的性能
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恩吉波尔作用于人类骨髓干细胞。

Engipore acts on human bone marrow stem cells.

作者信息

Sollazzo Vincenzo, Palmieri Annalisa, Girardi Ambra, Farinella Francesca, Carinci Francesco

机构信息

Orthopedic Clinic, University of Ferrara, Corso Giovecca 203, 44100 Ferrara, Italy.

出版信息

Saudi Dent J. 2010 Oct;22(4):161-6. doi: 10.1016/j.sdentj.2010.07.007. Epub 2010 Jul 17.

DOI:10.1016/j.sdentj.2010.07.007
PMID:23960492
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3723274/
Abstract

OBJECTIVES

Porous HA scaffolds are promising materials for tissue engineering because they offer a tridimensional support and serve as template for cell proliferation and at last tissue formation. Engipore provide a natural 3D scaffold with organic fibrous material in bone. However, how this material alters osteoblast activity to promote bone formation is poorly understood.

MATERIALS AND METHODS

To study how Engipore can induce osteoblast differentiation in mesenchymal stem cells, the expression levels of bone related genes and mesenchymal stem cells marker were analyzed.

RESULTS

Engipore causes a significant induction of osteoblast transcriptional factors like SP7 and RUNX2 and of the bone-related gene osteocalcin (BGLAP). The expression of CD105 was not significantly changed in stem cells treated with Engipore with respect to untreated cells, while SSP1 (osteopontin) was significantly down expressed thus reducing osteoclast activity.

CONCLUSIONS

The obtained results can be relevant to better understand the molecular mechanism of bone regeneration.

摘要

目的

多孔羟基磷灰石支架是组织工程中有前景的材料,因为它们提供三维支撑,并作为细胞增殖及最终组织形成的模板。Engipore在骨中提供一种含有有机纤维材料的天然三维支架。然而,这种材料如何改变成骨细胞活性以促进骨形成却知之甚少。

材料与方法

为研究Engipore如何诱导间充质干细胞向成骨细胞分化,分析了骨相关基因和间充质干细胞标志物的表达水平。

结果

Engipore能显著诱导成骨细胞转录因子如SP7和RUNX2以及骨相关基因骨钙素(BGLAP)的表达。与未处理细胞相比,用Engipore处理的干细胞中CD105的表达没有显著变化,而骨桥蛋白(SSP1)显著下调,从而降低破骨细胞活性。

结论

所获得的结果可能有助于更好地理解骨再生的分子机制。