Human stem cells from the apical papilla response to bacterial lipopolysaccharide exposure and anti-inflammatory effects of nuclear factor I C.
Human stem cells from the apical papilla response to bacterial lipopolysaccharide exposure and anti-inflammatory effects of nuclear factor I C.
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来自根尖乳头的人类干细胞对细菌脂多糖暴露的反应和核因子 I C 的抗炎作用。
DOI：
10.1016/j.joen.2013.07.018
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发表时间：
2013-11
影响因子：
4.2
通讯作者：
Smith, Anthony J
中科院分区：
文献类型：
--
作者：
He, Wenxi;Zhang, Yaqing;Lv, Haipeng;Yu, Qing;Zhou, Zeyuan;Zhu, Qinglin;Wang, Zhihua;Cooper, Paul R;Smith, Anthony J
根尖乳头干细胞（stem cells from apical papilla，SCAPs）是牙根发育的重要细胞，可能成为未成熟牙齿再生牙髓手术的候选细胞。SCAPs在临床应用中的潜在用途需要更好地了解其对细菌挑战的反应。我们研究了这些细胞暴露于脂多糖（LPS）的影响。由细菌挑战引起的炎症反应可以限制损伤后组织再生和核因子I C（NFIC）的作用，其在牙根发育中起关键作用。NFIC已探讨其抗炎作用的背景下，牙髓治疗的未成熟的牙齿，继续根发育是一个重要outcome.MethodsSCAPs暴露于LPS，Toll样受体4（TLR 4），白细胞介素（IL）-6，IL-8和肿瘤坏死因子（TNF-α）的表达进行了评估，通过实时聚合酶链反应（RT-PCR）。通过Western blotting或RT-PCR检测编码SCAPs中全长NFIC或siRNA沉默NFIC的pLenti6.3/v5-NFIC质粒;通过RT-PCR分析NFIC对IL-6、IL-8和TNF-α的影响。结果LPS可诱导SCAPs合成IL-6、IL-8和TNF-α，并呈时间依赖性。用TLR 4抑制剂预处理显著抑制LPS诱导的IL-6、IL-8和TNF-α表达。敲低NFIC可增加IL-6、IL-8和TNF-α的表达，而过表达NFIC可抑制1 μg/mL LPS刺激的炎症反应，尤其是IL-8。总之，这些数据表明，LPS是公认的跨膜受体TLR 4介导炎症反应的SCAPs和NFIC过表达可以抑制LPS引发的先天性免疫responses.ConclusionsThe抗炎作用的NFIC过表达提供了一个有价值的目标，以抑制炎症反应在受感染的纸浆，让组织再生发生。
IntroductionStem cells from the apical papilla (SCAPs) are important for tooth root development and may be candidates for regenerative endodontic procedures involving immature teeth. The potential use of SCAPs for clinical applications requires a better understanding of their responses to bacterial challenge. We have investigated the effects of exposure of these cells to lipopolysaccharide (LPS). Inflammatory responses arising from bacterial challenges can constrain postinjury tissue regeneration and the effects of nuclear factor I C (NFIC), which plays a critical role in tooth root development. NFIC has been explored for its anti-inflammatory action in the context of endodontic treatment of immature teeth where continued root development is an important outcome.MethodsSCAPs were exposed to LPS, and the expression of Toll-like receptor-4 (TLR4), interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF-α) were assessed by real-time polymerase chain reaction (RT-PCR). The pLenti6.3/v5-NFIC plasmid encoding the full-length NFIC or NFIC silencing by si-RNA (small interfering RNA) in SCAPs were measured by Western blotting or RT-PCR; the effects of NFIC on IL-6, IL-8, and TNF-α were analyzed by RT-PCR. The protein levels were subsequently measured by enzyme-linked immunoassay.ResultsLPS induced the synthesis of IL-6, IL-8, and TNF-α in SCAPs in a time-dependent manner. Pretreatment with a TLR4 inhibitor significantly inhibited LPS-induced IL-6, IL-8, and TNF-α expression. Knockdown of NFIC increased the expression of IL-6, IL-8, and TNF-α, whereas the overexpression of NFIC resulted in the suppression of the inflammatory response stimulated by 1 μg/mL LPS, especially for IL-8. Together, these data show that LPS is recognized by the transmembranous receptor TLR4 to mediate inflammatory responses in SCAPs and NFIC overexpression can suppress LPS-initiated innate immune responses.ConclusionsThe anti-inflammatory effects of NFIC overexpression provide a valuable target to dampen inflammatory responses in the infected pulp to allow tissue regeneration to occur.
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影响因子：
3.8
作者：
F. Rougier;Elisabeth Cornu;Vincent Praloran;Yves Denizot
通讯作者：
F. Rougier;Elisabeth Cornu;Vincent Praloran;Yves Denizot
DOI：
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发表时间：
--
期刊：
--
影响因子：
--
作者：
通讯作者：
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DOI：
10.1073/pnas.79.21.6438
发表时间：
1982-01-01
期刊：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES
影响因子：
--
作者：
NAGATA, K;GUGGENHEIMER, RA;HURWITZ, J
通讯作者：
HURWITZ, J
影响因子：
6.1
作者：
Huan-Tian Zhang;Z. Zha;Jia-hui Cao;Zu-jian Liang;Haoming Wu;M. He;X. Zang;Ping Yao;Jiaqing Zhang
通讯作者：
Huan-Tian Zhang;Z. Zha;Jia-hui Cao;Zu-jian Liang;Haoming Wu;M. He;X. Zang;Ping Yao;Jiaqing Zhang
影响因子：
4.2
作者：
S. Oliveira;V. A. C. Santos
通讯作者：
S. Oliveira;V. A. C. Santos