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CTHRC1通过调控TAZ促进牙周膜干细胞的成骨分化。

CTHRC1 promotes osteogenic differentiation of periodontal ligament stem cells by regulating TAZ.

作者信息

Wang Chengze, Gu Weiting, Sun Baiyu, Zhang Yunpeng, Ji Yawen, Xu Xin, Wen Yong

机构信息

School of Stomatology, Shandong University, No. 44-1, Wenhua Xi Road, Jinan, 250012, Shandong, People's Republic of China.

Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Jinan, People's Republic of China.

出版信息

J Mol Histol. 2017 Aug;48(4):311-319. doi: 10.1007/s10735-017-9729-0. Epub 2017 Jun 24.

Abstract

Collagen triple helix repeat containing 1 (CTHRC1) is associated with bone metabolism. Alveolar bone has an ability to rapidly remodel itself to adapt its biomechanical environment and function. However, whether CTHRC1 is expressed in alveolar bone tissue and the role of CTHRC1 in alveolar bone remodeling remain unclear. We used orthodontic tooth movement (OTM) rat model to study the effects of CHTRC1 in alveolar bone remodeling in vivo. We found that CTHRC1 was expressed in normal physiological condition of osteocytes, bone matrix, and periodontal ligament cells in rat. During the OTM, the expression of CTHRC1, Runx2 and TAZ were increased. We further studied the effects of CTHRC1 on osteogenic differentiation of human periodontal ligament stem cells in vitro. CTHRC1 can positively regulate the expression of TAZ and osteogenic differentiation markers like Col1, ALP, Runx2 and OCN. Overexpression of CHTRC1 increased osteogenic differentiation of PDLSCs, which could be abolished by TAZ siRNA. Our results suggest that CTHRC1 plays an important role in alveolar bone remodeling and osteogenic differentiation of PDLSCs.

摘要

含胶原蛋白三螺旋重复序列1(CTHRC1)与骨代谢相关。牙槽骨具有快速自我重塑以适应其生物力学环境和功能的能力。然而,CTHRC1是否在牙槽骨组织中表达以及CTHRC1在牙槽骨重塑中的作用仍不清楚。我们使用正畸牙齿移动(OTM)大鼠模型来研究CHTRC1在体内牙槽骨重塑中的作用。我们发现CTHRC1在大鼠骨细胞、骨基质和牙周膜细胞正常生理状态下表达。在OTM过程中,CTHRC1、Runx2和TAZ的表达增加。我们进一步研究了CTHRC1对人牙周膜干细胞体外成骨分化的影响。CTHRC1可正向调节TAZ以及成骨分化标志物如Col1、ALP、Runx2和OCN的表达。CHTRC1的过表达增加了PDLSCs的成骨分化,而TAZ siRNA可消除这种作用。我们的结果表明CTHRC1在牙槽骨重塑和PDLSCs的成骨分化中起重要作用。

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