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炎症牙周组织中的趋化因子激活健康牙周韧带干细胞的迁移。

Chemokine in inflamed periodontal tissues activates healthy periodontal-ligament stem cell migration.

机构信息

Department of Periodontology, Research Institute for Periodontal Regeneration, College of Dentistry, Yonsei University, Seoul, Korea.

Department of Applied Life Science, BK21 PLUS Project, College of Dentistry, Yonsei University, Seoul, Korea.

出版信息

J Clin Periodontol. 2017 May;44(5):530-539. doi: 10.1111/jcpe.12710. Epub 2017 Mar 31.

Abstract

AIM

The present study aimed to characterize the expression pattern of chemokines obtained from inflamed periodontal defects and to determine the characteristics of human periodontal-ligament stem cells (hPDLSCs) migrated by each specific chemokine.

MATERIALS AND METHODS

Both inflamed and healthy periodontal tissues were obtained from periodontitis patients (n = 11), and the chemokine expression levels were analyzed. The periodontal-tissue-specific chemokines were applied to healthy hPDLSCs from extracted teeth (n = 3), with FGF-2 acting as a positive control. Cells were separated by selected chemokines using transwell method into migrated/unmigrated hPDLSCs. The characteristics of the hPDLSC subpopulation recruited by each chemokine were assessed, and gene expression pattern was analyzed by microarray.

RESULTS

Chemokines were categorized into three groups by specific patterns of "appearing," "increasing," and "decreasing/disappearing" from healthy to inflamed tissues. A representative chemokine from each group enhanced the capacities for colony formation and osteogenic/adipogenic differentiation while maintaining the surface markers of hPDLSCs. RANTES/CCL5 significantly increased the cellular migration of hPDLSCs, via enhancement of signaling pathways, regulation of the actin skeleton, and focal adhesion.

CONCLUSION

The present study found a specific chemokine profile induced by inflammation in periodontal tissues, with RANTES/CCL5 appearing to play a role in the migration of hPDLSCs into inflammatory periodontal lesions.

摘要

目的

本研究旨在分析炎症性牙周缺损来源的趋化因子的表达模式,并确定每种趋化因子所趋化的人牙周韧带干细胞(hPDLSCs)的特性。

材料和方法

从牙周炎患者(n=11)中获取炎症和健康的牙周组织,分析趋化因子的表达水平。将牙周组织特异性趋化因子应用于从拔牙中提取的健康 hPDLSCs(n=3),以 FGF-2 作为阳性对照。采用transwell 法,用选定的趋化因子将细胞分为迁移/未迁移的 hPDLSCs。评估每种趋化因子募集的 hPDLSC 亚群的特征,并通过微阵列分析基因表达模式。

结果

趋化因子根据从健康到炎症组织的特定“出现”、“增加”和“减少/消失”模式分为三组。每组的代表性趋化因子增强了集落形成和成骨/成脂分化的能力,同时保持 hPDLSCs 的表面标记。RANTES/CCL5 通过增强信号通路、调节肌动蛋白骨架和黏附斑,显著增加 hPDLSCs 的细胞迁移。

结论

本研究发现了牙周组织炎症诱导的特定趋化因子谱,RANTES/CCL5 似乎在 hPDLSCs 迁移到炎症性牙周病变中起作用。

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