IL-1 Receptor Antagonist Protects the Osteogenesis Capability of Gingival-Derived Stem/Progenitor Cells under Inflammatory Microenvironment Induced by Porphyromonas gingivalis Lipopolysaccharides

牙龈卟啉单胞菌 间充质干细胞 促炎细胞因子 化学 干细胞 炎症 细胞因子 TLR4型 脂多糖 免疫学 牙周炎 细胞生物学 生物 医学 内科学
作者
Yuxin Zhao,Bobo Cai,Weijun Zhu,Jue Shi,Yu Wang,Misi Si
出处
期刊:Stem Cells International [Hindawi Publishing Corporation]
卷期号:2021: 1-14 被引量:9
标识
DOI:10.1155/2021/6638575
摘要

Mesenchymal stem cells (MSCs) have been considered to be a future treatment option for periodontitis due to their excellent regenerative capability. However, it is still a challenge to protect MSCs’ biological properties from multiple bacterial toxins in local inflammatory environment. The present study is aimed at investigating the treatment effect of interleukin-1 receptor antagonist (IL-1ra) on cell proliferation, migration, and osteogenic differentiation of gingival-derived mesenchymal stem cells (GMSCs) under an inflammatory microenvironment induced by Porphyromonas gingivalis lipopolysaccharides (P. gingivalis-LPS). GMSCs derived from Sprague-Dawley (SD) rats’ free gingival tissues were treated with P. gingivalis-LPS (10 μg/mL) to create in vitro inflammatory environment. Different concentrations of IL-1ra (0.01-1 μg/mL) were used to antagonize the negative effect of LPS. Cell behaviors including proliferation, cloning formation unit (CFU), cell migration, osteogenic differentiation, mineral deposition, and cytokine production were assessed to investigate the protection effect of IL-1ra on GMSCs under inflammation. The toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) pathway activated by LPS was evaluated by real-time quantitative polymerase chain reaction (RT-PCR) and western blot. In response to P. gingivalis-LPS treatment, cell numbers, cloning formation rate, cell migration rate, proinflammatory cytokine production, and osteogenic differentiation-associated protein/mRNA expressions as well as mineralized nodules were suppressed in a time-dependent manner. These negative effects were effectively attenuated by IL-1ra administration in a time- and dose-dependent manner. In addition, mRNA expressions of TLR4 and IkBα decreased dramatically when IL-1ra was added into LPS-induced medium. IL-1ra also reversed the LPS-induced TLR4/NF-κB activation as indicated by western blot. The present study revealed that IL-1ra decreased inflammatory cytokine production in a supernatant, so as to protect GMSCs’ osteogenesis capacity and other biological properties under P. gingivalis-LPS-induced inflammatory environment. This might be explained by IL-1ra downregulating TLR4-mediated NF-κB signaling pathway activation.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
2秒前
2秒前
彭于晏应助duran采纳,获得10
2秒前
4秒前
不敢装睡发布了新的文献求助10
4秒前
彩虹大侠发布了新的文献求助10
5秒前
halosheep完成签到,获得积分10
5秒前
5秒前
duanhahaha完成签到,获得积分10
6秒前
夏东方完成签到,获得积分20
6秒前
6秒前
赵磊完成签到,获得积分10
7秒前
大个应助aspirin采纳,获得10
7秒前
www999完成签到,获得积分10
8秒前
李健的小迷弟应助5430采纳,获得10
8秒前
shidewu完成签到,获得积分10
8秒前
情怀应助Allure采纳,获得10
9秒前
朱艺发布了新的文献求助10
9秒前
CipherSage应助星河在眼里采纳,获得10
10秒前
量子星尘发布了新的文献求助10
10秒前
10秒前
11秒前
达进发布了新的文献求助10
11秒前
12秒前
奋斗龙猫发布了新的文献求助10
12秒前
13秒前
英姑应助小超人采纳,获得10
14秒前
桐桐应助达进采纳,获得10
14秒前
科研通AI2S应助难寻采纳,获得10
15秒前
吴可之完成签到,获得积分10
15秒前
16秒前
16秒前
16秒前
王大壮完成签到,获得积分10
16秒前
你好啊发布了新的文献求助10
17秒前
一一应助长孙天寿采纳,获得20
18秒前
fy发布了新的文献求助10
18秒前
18秒前
WAWA发布了新的文献求助10
19秒前
kxdr发布了新的文献求助10
20秒前
高分求助中
【提示信息,请勿应助】请使用合适的网盘上传文件 10000
Continuum Thermodynamics and Material Modelling 2000
Chinesen in Europa – Europäer in China: Journalisten, Spione, Studenten 1200
Deutsche in China 1920-1950 1200
Electron microscopy study of magnesium hydride (MgH2) for Hydrogen Storage 800
Green Star Japan: Esperanto and the International Language Question, 1880–1945 800
Sentimental Republic: Chinese Intellectuals and the Maoist Past 800
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 物理 生物化学 纳米技术 计算机科学 化学工程 内科学 复合材料 物理化学 电极 遗传学 量子力学 基因 冶金 催化作用
热门帖子
关注 科研通微信公众号,转发送积分 3871052
求助须知:如何正确求助?哪些是违规求助? 3413160
关于积分的说明 10683368
捐赠科研通 3137607
什么是DOI,文献DOI怎么找? 1731128
邀请新用户注册赠送积分活动 834579
科研通“疑难数据库(出版商)”最低求助积分说明 781223