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基质细胞衍生因子-1/Exendin-4 联合治疗促进体外人牙周韧带干细胞的增殖、迁移和成骨分化，并促进体内牙周骨再生。

Stromal cell-derived factor-1/Exendin-4 cotherapy facilitates the proliferation, migration and osteogenic differentiation of human periodontal ligament stem cells in vitro and promotes periodontal bone regeneration in vivo.

机构信息

Department of Periodontology, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, Jinan Shandong, China.

Department of Stomatology, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan Shandong, China.

出版信息

Cell Prolif. 2021 Mar;54(3):e12997. doi: 10.1111/cpr.12997. Epub 2021 Jan 29.

DOI:10.1111/cpr.12997
PMID:33511708
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7941242/
Abstract

OBJECTIVES

Stromal cell-derived factor-1 (SDF-1) actively directs endogenous cell homing. Exendin-4 (EX-4) promotes stem cell osteogenic differentiation. Studies revealed that EX-4 strengthened SDF-1-mediated stem cell migration. However, the effects of SDF-1 and EX-4 on periodontal ligament stem cells (PDLSCs) and bone regeneration have not been investigated. In this study, we aimed to evaluate the effects of SDF-1/EX-4 cotherapy on PDLSCs in vitro and periodontal bone regeneration in vivo.

METHODS

Cell-counting kit-8 (CCK8), transwell assay, qRT-PCR and western blot were used to determine the effects and mechanism of SDF-1/EX-4 cotherapy on PDLSCs in vitro. A rat periodontal bone defect model was developed to evaluate the effects of topical application of SDF-1 and systemic injection of EX-4 on endogenous cell recruitment, osteoclastogenesis and bone regeneration in vivo.

RESULTS

SDF-1/EX-4 cotherapy had additive effects on PDLSC proliferation, migration, alkaline phosphatase (ALP) activity, mineral deposition and osteogenesis-related gene expression compared to SDF-1 or EX-4 in vitro. Pretreatment with ERK inhibitor U0126 blocked SDF-1/EX-4 cotherapy induced ERK signal activation and PDLSC proliferation. SDF-1/EX-4 cotherapy significantly promoted new bone formation, recruited more CXCR4 cells and CD90 /CD34 stromal cells to the defects, enhanced early-stage osteoclastogenesis and osteogenesis-related markers expression in regenerated bone compared to control, SDF-1 or EX-4 in vivo.

CONCLUSIONS

SDF-1/EX-4 cotherapy synergistically regulated PDLSC activities, promoted periodontal bone formation, thereby providing a new strategy for periodontal bone regeneration.

摘要

目的

基质细胞衍生因子-1（SDF-1）积极指导内源性细胞归巢。Exendin-4（EX-4）促进干细胞成骨分化。研究表明，EX-4 增强了 SDF-1 介导的干细胞迁移。然而，SDF-1 和 EX-4 对牙周韧带干细胞（PDLSCs）和骨再生的影响尚未得到研究。在本研究中，我们旨在评估 SDF-1/EX-4 联合治疗对体外 PDLSCs 和体内牙周骨再生的影响。

方法

使用细胞计数试剂盒-8（CCK8）、Transwell 测定、qRT-PCR 和 Western blot 来确定 SDF-1/EX-4 联合治疗对体外 PDLSCs 的影响和机制。建立大鼠牙周骨缺损模型，评估 SDF-1 局部应用和 EX-4 全身注射对体内内源性细胞募集、破骨细胞生成和骨再生的影响。

结果

与 SDF-1 或 EX-4 相比，SDF-1/EX-4 联合治疗在体外对 PDLSC 增殖、迁移、碱性磷酸酶（ALP）活性、矿化沉积和成骨相关基因表达具有相加作用。ERK 抑制剂 U0126 预处理阻断了 SDF-1/EX-4 联合治疗诱导的 ERK 信号激活和 PDLSC 增殖。与对照组、SDF-1 或 EX-4 相比，SDF-1/EX-4 联合治疗显著促进新骨形成，募集更多 CXCR4 细胞和 CD90/CD34 基质细胞到缺损处，增强早期破骨细胞生成和再生骨中成骨相关标志物的表达。

结论

SDF-1/EX-4 联合治疗协同调节 PDLSC 活性，促进牙周骨形成，为牙周骨再生提供了一种新策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad99/7941242/8c1fee56d4d2/CPR-54-e12997-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad99/7941242/3867e0397b78/CPR-54-e12997-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad99/7941242/abe128b81a7d/CPR-54-e12997-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad99/7941242/ae59fdfec4f1/CPR-54-e12997-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad99/7941242/e98a6caff1d1/CPR-54-e12997-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad99/7941242/3867e0397b78/CPR-54-e12997-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad99/7941242/015cc82d7512/CPR-54-e12997-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad99/7941242/7636cd22e01a/CPR-54-e12997-g010.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad99/7941242/8c1fee56d4d2/CPR-54-e12997-g003.jpg

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