干细胞领域知识发现平台

提升科研信息化水平
支撑研究所科技创新

  融合多源信息    打通数据孤岛
  挖掘知识关联    放大数据价值
  集成知识计算    促进知识发现

免费注册账号
查看全文和研发动态、知识导航以及收藏您喜欢的数据等操作,您需要注册一个免费帐户并登录。

写笔记

您最近的笔记
The osteogenic differentiation of PDLSCs is mediated through MEK/ERK and p38 MAPK signalling under hypoxia
Archives of Oral Biology, Issue: 10, Volume: 58, Pages: 1357-1368. | 2013-01-10
0 Patent citations    21 Scholarly citations     Reference Count: 49
Yeke Wu;Yunqiang Yang;Pu Yang;Yifei Gu;Zhihe Zhao;Lijun Tan;Lixing Zhao;Tian Tang;Yu Li

摘要

Abstract Purpose During orthodontic treatment and chronic periodontitis, the periodontal vasculature is severely impaired by overloaded mechanical force or chronic inflammation. This leads to the hypoxic milieu of the periodontal stem cell niche and ultimately affects periodontal tissue remodelling. However, the role of hypoxia in the regulation of periodontal ligament stem cell (PDLSC) behaviours still remains to be elucidated. The present study was aimed at investigating the effects of hypoxia on osteogenic differentiation, mineralisation and paracrine release of PDLSCs and further demonstrating the involvement of mitogen-activated protein kinase (MAPK) signalling in the process. Methods First, PDLSCs were isolated and characterised. Second, the effects of different periods of hypoxia on PDLSC osteogenic potential, mineralisation and paracrine release were investigated. Third, extracellular signal-regulated kinases 1 and 2 (ERK1/2) and p38 kinase activities under hypoxia were measured. Finally, specific MAPK inhibitors PD98059 and SB203580 were employed to investigate the involvement of two kinases in PDLSC osteogenesis under hypoxia. Results Immunocytochemical staining and multilineage differentiation assays verified that the isolated cells were PDLSCs. Cell viability, alkaline phosphatase (ALP) activity, messenger RNA (mRNA) and protein levels of runt-related transcription factor 2 (Runx2) and Sp7, mineralisation and prostaglandin E2 (PGE 2 ) and vascular endothelial growth factor (VEGF) release were significantly increased by hypoxia. ERK1/2 and p38 were activated in different ways under hypoxia. Furthermore, hypoxia-stimulated transcription and expression of the above-mentioned osteogenic regulators were also reversed by PD98059 and SB203580 to different degrees. Conclusions Exposure of PDLSCs to hypoxia affected their osteogenic potential, mineralisation and paracrine release, and the process involved mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (MEK/ERK) and p38 MAPK signalling.


机构

Sichuan University;State Key Laboratory of Oral Diseases, Department of Orthodontics, West China Hospital of Stomatology, Sichuan University, No. 14, 3rd Section, Renmin South Road, Chengdu 610041, PR China.Huazhong University of Science and TechnologySichuan UniversitySichuan UniversitySichuan UniversitySichuan UniversitySichuan UniversitySichuan UniversitySichuan University


文献类型:

journal article;research support, non-u.s. gov't;

出版商:

Elsevier Limited

发表时间:

2013-01-10

基金信息

National Natural Science Foundation of China()