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Lipopolysaccharide from Escherichia coli stimulates osteogenic differentiation of human periodontal ligament stem cells through Wnt/β-catenin-induced TAZ elevation.
Molecular Oral Microbiology ( IF 3.7 ) Pub Date : 2018-12-11 , DOI: 10.1111/omi.12249
Yixiao Xing 1, 2 , Yunpeng Zhang 1, 2 , Linglu Jia 1, 2 , Xin Xu 1, 2
Affiliation  

Human periodontal ligament stem cells (PDLSCs), a type of dental tissue–derived mesenchymal stem cells (MSCs), can be clinically applied in periodontal tissue regeneration to treat periodontitis, which is initiated and sustained by bacteria. Lipopolysaccharide (LPS), the major component of the outer membrane of gram‐negative bacteria, is a pertinent deleterious factor in the oral microenvironment. The aim of this study was to investigate the effect of LPS on the proliferation and osteogenic differentiation of PDLSCs, as well as the mechanisms involved. Proliferation and osteogenic differentiation of PDLSCs were detected under the stimulation of Escherichia coli–derived LPS. The data showed that E. coli–derived LPS did not affect the proliferation, viability, and cell cycle of PDLSCs. Furthermore, it promoted osteogenic differentiation with the activation of TAZ. Lentivirus‐mediated depletion of TAZ (transcriptional activator with a PDZ motif) was used to determine the role of TAZ on LPS‐induced enhancement of osteogenesis. PDLSCs cultured in osteogenic media with or without LPS and DKK1 (Wnt/β‐catenin pathway inhibitor) were used to determine the regulatory effect of Wnt signaling. We found that TAZ depletion offset LPS‐induced enhancement of osteogenesis. Moreover, treatment with DKK1 offset LPS‐induced TAZ elevation and osteogenic promotion. In conclusion, E. coli–derived LPS promoted osteogenic differentiation of PDLSCs by fortifying TAZ activity. The elevation and activation of TAZ were mostly mediated by the Wnt/β‐catenin pathway. PDLSC‐governed alveolar bone tissue regeneration was not necessarily reduced under bacterial conditions and could be modulated by Wnt and TAZ.

中文翻译:

大肠杆菌中的脂多糖通过Wnt /β-catenin诱导的TAZ升高刺激人牙周膜干细胞的成骨分化。

人牙周膜干细胞(PDLSC)是一种源自牙组织的间充质干细胞(MSC),可在临床上应用到牙周组织再生中,以治疗由细菌引发和维持的牙周炎。脂多糖(LPS)是革兰氏阴性细菌外膜的主要成分,是口腔微环境中的相关有害因素。这项研究的目的是调查LPS对PDLSCs增殖和成骨分化的影响,以及所涉及的机制。在大肠杆菌衍生的LPS的刺激下检测到PDLSCs的增殖和成骨分化。数据表明,大肠杆菌衍生的LPS不会影响PDLSC的增殖,生存能力和细胞周期。此外,它通过激活TAZ促进成骨分化。慢病毒介导的TAZ耗竭(具有PDZ图案的转录激活因子)用于确定TAZ在LPS诱导的成骨增强中的作用。在有或没有LPS和DKK1(Wnt /β-catenin途径抑制剂)的成骨培养基中培养的PDLSC用于确定Wnt信号的调节作用。我们发现,TAZ耗竭抵消了LPS诱导的成骨作用增强。此外,用DKK1治疗可抵消LPS诱导的TAZ升高和成骨促进作用。总之,大肠杆菌衍生的LPS通过增强TAZ活性来促进PDLSC的成骨分化。TAZ的升高和激活主要由Wnt /β-catenin途径介导。PDLSC控制的牙槽骨组织再生在细菌条件下并不一定会减少,并且可能受Wnt和TAZ调节。
更新日期:2018-12-11
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