IL-7通过失活丝裂原活化蛋白激酶途径抑制牙周韧带干细胞成骨分化。

IF 1.6 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Organogenesis Pub Date : 2016-10-01 Epub Date: 2016-08-31 DOI:10.1080/15476278.2016.1229726
Cong-Xiang Jian, Quan-Shui Fan, Yong-He Hu, Yong He, Ming-Zhe Li, Wei-Yin Zheng, Yu Ren, Chen-Jun Li
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引用次数: 9

摘要

牙周韧带干细胞(Periodontal ligament stem cells, PDLSCs)是组织特异性间充质干细胞(mesenchymal stem cells, MSCs),在牙齿缺失的再生治疗中具有重要作用。白细胞介素-7 (Interleukin-7, IL-7)是骨髓间充质干细胞等基质细胞产生的关键细胞因子,在多发性骨髓瘤的B细胞、T细胞发育和成骨细胞分化中具有特殊作用。然而,IL-7对PDLSCs成骨分化的影响尚不清楚。因此,在本研究中,我们在体外确定IL-7是否影响PDLSCs的增殖和成骨分化,并探索IL-7介导细胞分化的相关信号通路。结果表明,分离的人PDLSCs具有MSCs的特征,高表达CD90、CD44、CD105、CD29和CD73,几乎不表达CD34、CD45、CD11b、CD14和CD117。IL-7对PDLSCs的增殖无显著影响,但能抑制其成骨分化,抑制碱性磷酸酶(ALP)活性。定量逆转录聚合酶链反应(qRT-PCR)和Western blotting结果显示,IL-7显著降低Runx-2、SP7和骨钙素(OCN)的表达水平。进一步研究表明,IL-7对JNK、ERK1/2和p38蛋白的产生没有显著影响,但明显抑制了它们的磷酸化水平。这些数据表明,IL-7可能通过使丝裂原活化蛋白激酶(MAPK)信号通路失活来抑制PDLSCs的成骨分化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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IL-7 suppresses osteogenic differentiation of periodontal ligament stem cells through inactivation of mitogen-activated protein kinase pathway.

Periodontal ligament stem cells (PDLSCs) are tissue-specific mesenchymal stem cells (MSCs), having an important role in regenerative therapy for teeth loss. Interleukin-7 (IL-7) is a key cytokine produced by stromal cells including MSCs, and exhibits specific roles for B and T cell development and osteoblasts differentiation of multiple myeloma. However, the effect of IL-7 on osteogenic differentiation of PDLSCs remains unclear. Therefore, in the present study we determined whether IL-7 affects the proliferation and osteogenic differentiation of PDLSCs in vitro and explored the associated signaling pathways for IL-7-mediated cell differentiation. The results demonstrated that the isolated human PDLSCs possessed MSCs features, highly expressing CD90, CD44, CD105, CD29 and CD73, and almost did not expressed CD34, CD45, CD11b, CD14 and CD117. IL-7 could not significantly affect the proliferation of PDLSCs, but it decreased their osteogenic differentiation and inhibited alkaline phosphatase (ALP) activity. The results of quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting exhibited that the expression levels of Runx-2, SP7 and osteocalcin (OCN) were significantly reduced by IL-7. Further studies indicated that IL-7 did not significantly change JNK, ERK1/2 and p38 protein production, but markedly suppressed their phosphorylation levels. These data suggest that IL-7 inhibits the osteogenic differentiation of PDLSCs probably via inactivation of mitogen-activated protein kinase (MAPK) signaling pathway.

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来源期刊
Organogenesis
Organogenesis BIOCHEMISTRY & MOLECULAR BIOLOGY-DEVELOPMENTAL BIOLOGY
CiteScore
4.10
自引率
4.30%
发文量
6
审稿时长
>12 weeks
期刊介绍: Organogenesis is a peer-reviewed journal, available in print and online, that publishes significant advances on all aspects of organ development. The journal covers organogenesis in all multi-cellular organisms and also includes research into tissue engineering, artificial organs and organ substitutes. The overriding criteria for publication in Organogenesis are originality, scientific merit and general interest. The audience of the journal consists primarily of researchers and advanced students of anatomy, developmental biology and tissue engineering. The emphasis of the journal is on experimental papers (full-length and brief communications), but it will also publish reviews, hypotheses and commentaries. The Editors encourage the submission of addenda, which are essentially auto-commentaries on significant research recently published elsewhere with additional insights, new interpretations or speculations on a relevant topic. If you have interesting data or an original hypothesis about organ development or artificial organs, please send a pre-submission inquiry to the Editor-in-Chief. You will normally receive a reply within days. All manuscripts will be subjected to peer review, and accepted manuscripts will be posted to the electronic site of the journal immediately and will appear in print at the earliest opportunity thereafter.
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