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The use of TLR2 modified BMSCs for enhanced bone regeneration in the inflammatory micro-environment.

Identifieur interne : 000054 ( Main/Exploration ); précédent : 000053; suivant : 000055

The use of TLR2 modified BMSCs for enhanced bone regeneration in the inflammatory micro-environment.

Auteurs : Qin Zhou [République populaire de Chine] ; Xiaoyu Gu [République populaire de Chine] ; Jiachen Dong [République populaire de Chine] ; Chao Zhu [République populaire de Chine] ; Zhen Cai [République populaire de Chine] ; Dongmei He [République populaire de Chine] ; Chi Yang [République populaire de Chine] ; Ling Xu [République populaire de Chine] ; Jiawei Zheng [République populaire de Chine]

Source :

RBID : pubmed:31387403

Descripteurs français

English descriptors

Abstract

The repair of periodontal bone tissue defects in patients with periodontitis is one of the major challenges for dentists. Stem cell-based bone regeneration has been considered as a promising strategy to restore the lost periodontal bone tissue. However, the local inflammatory environment of periodontal tissue affects stem cell-based periodontal bone regeneration. Toll-like receptor 2 (TLR2), a member of the TLR family, plays an important role in regulating immunoreaction. Previous studies have shown that the activation of TLR2 signaling pathway is involved in enhancing tissue vascularization and wound healing. However, the mechanisms underlying the therapeutic effects of TLR2 on regulating bone marrow stromal cells (BMSCs) mediated periodontal bone tissue regeneration still need to be further investigated. In this study, we tested the effect of TLR2 on regulating BMSCs mediated alveolar bone regeneration by establishing a TLR2 gene-modified canine BMSCs using a lentivirus. Activation of TLR2 significantly enhanced the expression of hypoxia-inducible factor-1α (HIF-1α) and bone morphogenetic protein 2 (BMP-2) and then upregulated the expression of their downstream osteogenic and angiogenic related gene in BMSCs. TLR2-BMSCs mediated bone regeneration in canine tooth extraction sockets under an inflammatory environment demonstrated that activation of the TLR2 signaling pathway significantly stimulated BMSCs meditated angiogenesis and osteogenesis.

DOI: 10.1080/21691401.2019.1626867
PubMed: 31387403


Affiliations:


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Le document en format XML

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<term>Animals (MeSH)</term>
<term>Bone Regeneration (MeSH)</term>
<term>Cell Differentiation (MeSH)</term>
<term>Cellular Microenvironment (MeSH)</term>
<term>Dogs (MeSH)</term>
<term>Inflammation (metabolism)</term>
<term>Inflammation (pathology)</term>
<term>Inflammation (physiopathology)</term>
<term>Male (MeSH)</term>
<term>Mesenchymal Stem Cell Transplantation (MeSH)</term>
<term>Mesenchymal Stem Cells (cytology)</term>
<term>Mesenchymal Stem Cells (metabolism)</term>
<term>Neovascularization, Physiologic (MeSH)</term>
<term>Osteogenesis (MeSH)</term>
<term>Signal Transduction (MeSH)</term>
<term>Toll-Like Receptor 2 (genetics)</term>
<term>Toll-Like Receptor 2 (metabolism)</term>
<term>Tooth Socket (diagnostic imaging)</term>
<term>Tooth Socket (metabolism)</term>
<term>Tooth Socket (pathology)</term>
<term>Tooth Socket (physiopathology)</term>
<term>X-Ray Microtomography (MeSH)</term>
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<term>Alvéole dentaire (anatomopathologie)</term>
<term>Alvéole dentaire (imagerie diagnostique)</term>
<term>Alvéole dentaire (métabolisme)</term>
<term>Alvéole dentaire (physiopathologie)</term>
<term>Animaux (MeSH)</term>
<term>Cellules souches mésenchymateuses (cytologie)</term>
<term>Cellules souches mésenchymateuses (métabolisme)</term>
<term>Chiens (MeSH)</term>
<term>Différenciation cellulaire (MeSH)</term>
<term>Inflammation (anatomopathologie)</term>
<term>Inflammation (métabolisme)</term>
<term>Inflammation (physiopathologie)</term>
<term>Microenvironnement cellulaire (MeSH)</term>
<term>Microtomographie aux rayons X (MeSH)</term>
<term>Mâle (MeSH)</term>
<term>Néovascularisation physiologique (MeSH)</term>
<term>Ostéogenèse (MeSH)</term>
<term>Récepteur de type Toll-2 (génétique)</term>
<term>Récepteur de type Toll-2 (métabolisme)</term>
<term>Régénération osseuse (MeSH)</term>
<term>Transduction du signal (MeSH)</term>
<term>Transplantation de cellules souches mésenchymateuses (MeSH)</term>
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<term>Tooth Socket</term>
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<term>Récepteur de type Toll-2</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en">
<term>Inflammation</term>
<term>Mesenchymal Stem Cells</term>
<term>Toll-Like Receptor 2</term>
<term>Tooth Socket</term>
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<term>Alvéole dentaire</term>
<term>Cellules souches mésenchymateuses</term>
<term>Inflammation</term>
<term>Récepteur de type Toll-2</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en">
<term>Inflammation</term>
<term>Tooth Socket</term>
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<term>Alvéole dentaire</term>
<term>Inflammation</term>
</keywords>
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<term>Inflammation</term>
<term>Tooth Socket</term>
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<term>Bone Regeneration</term>
<term>Cell Differentiation</term>
<term>Cellular Microenvironment</term>
<term>Dogs</term>
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<term>Microtomographie aux rayons X</term>
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<term>Ostéogenèse</term>
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<div type="abstract" xml:lang="en">The repair of periodontal bone tissue defects in patients with periodontitis is one of the major challenges for dentists. Stem cell-based bone regeneration has been considered as a promising strategy to restore the lost periodontal bone tissue. However, the local inflammatory environment of periodontal tissue affects stem cell-based periodontal bone regeneration. Toll-like receptor 2 (TLR2), a member of the TLR family, plays an important role in regulating immunoreaction. Previous studies have shown that the activation of TLR2 signaling pathway is involved in enhancing tissue vascularization and wound healing. However, the mechanisms underlying the therapeutic effects of TLR2 on regulating bone marrow stromal cells (BMSCs) mediated periodontal bone tissue regeneration still need to be further investigated. In this study, we tested the effect of TLR2 on regulating BMSCs mediated alveolar bone regeneration by establishing a TLR2 gene-modified canine BMSCs using a lentivirus. Activation of TLR2 significantly enhanced the expression of hypoxia-inducible factor-1α (HIF-1α) and bone morphogenetic protein 2 (BMP-2) and then upregulated the expression of their downstream osteogenic and angiogenic related gene in BMSCs. TLR2-BMSCs mediated bone regeneration in canine tooth extraction sockets under an inflammatory environment demonstrated that activation of the TLR2 signaling pathway significantly stimulated BMSCs meditated angiogenesis and osteogenesis.</div>
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<AbstractText>The repair of periodontal bone tissue defects in patients with periodontitis is one of the major challenges for dentists. Stem cell-based bone regeneration has been considered as a promising strategy to restore the lost periodontal bone tissue. However, the local inflammatory environment of periodontal tissue affects stem cell-based periodontal bone regeneration. Toll-like receptor 2 (TLR2), a member of the TLR family, plays an important role in regulating immunoreaction. Previous studies have shown that the activation of TLR2 signaling pathway is involved in enhancing tissue vascularization and wound healing. However, the mechanisms underlying the therapeutic effects of TLR2 on regulating bone marrow stromal cells (BMSCs) mediated periodontal bone tissue regeneration still need to be further investigated. In this study, we tested the effect of TLR2 on regulating BMSCs mediated alveolar bone regeneration by establishing a TLR2 gene-modified canine BMSCs using a lentivirus. Activation of TLR2 significantly enhanced the expression of hypoxia-inducible factor-1α (HIF-1α) and bone morphogenetic protein 2 (BMP-2) and then upregulated the expression of their downstream osteogenic and angiogenic related gene in BMSCs. TLR2-BMSCs mediated bone regeneration in canine tooth extraction sockets under an inflammatory environment demonstrated that activation of the TLR2 signaling pathway significantly stimulated BMSCs meditated angiogenesis and osteogenesis.</AbstractText>
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<Affiliation>d Department of Oral and Maxillofacial Surgery, Shandong Linyi People's Hospital , Linyi , China.</Affiliation>
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<Affiliation>a Department of Oral and Maxillofacial Surgery, Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine , Shanghai , China.</Affiliation>
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<Affiliation>b Department of Prothodontics, Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine , Shanghai , China.</Affiliation>
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<Affiliation>e Shanghai Key Laboratory of Stomatology and Shanghai Research Institute of Stomatology, National Clinical Research Center of Stomatology , Shanghai , China.</Affiliation>
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<AffiliationInfo>
<Affiliation>a Department of Oral and Maxillofacial Surgery, Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine , Shanghai , China.</Affiliation>
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<Country>England</Country>
<MedlineTA>Artif Cells Nanomed Biotechnol</MedlineTA>
<NlmUniqueID>101594777</NlmUniqueID>
<ISSNLinking>2169-1401</ISSNLinking>
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<ChemicalList>
<Chemical>
<RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D051195">Toll-Like Receptor 2</NameOfSubstance>
</Chemical>
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<DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
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<MeshHeading>
<DescriptorName UI="D001861" MajorTopicYN="Y">Bone Regeneration</DescriptorName>
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<DescriptorName UI="D059630" MajorTopicYN="N">Mesenchymal Stem Cells</DescriptorName>
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<DescriptorName UI="D020390" MajorTopicYN="N">Tooth Socket</DescriptorName>
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</MeshHeading>
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<DescriptorName UI="D055114" MajorTopicYN="N">X-Ray Microtomography</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM">
<Keyword MajorTopicYN="N">BMSCs</Keyword>
<Keyword MajorTopicYN="N">TLR2</Keyword>
<Keyword MajorTopicYN="N">inflammatory</Keyword>
<Keyword MajorTopicYN="N">micro-environment</Keyword>
<Keyword MajorTopicYN="N">periodontal bone regeneration</Keyword>
</KeywordList>
</MedlineCitation>
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<Year>2019</Year>
<Month>8</Month>
<Day>8</Day>
<Hour>6</Hour>
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<Day>8</Day>
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<Year>2019</Year>
<Month>12</Month>
<Day>31</Day>
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<PublicationStatus>ppublish</PublicationStatus>
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<ArticleId IdType="pubmed">31387403</ArticleId>
<ArticleId IdType="doi">10.1080/21691401.2019.1626867</ArticleId>
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<country>
<li>République populaire de Chine</li>
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<country name="République populaire de Chine">
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<name sortKey="Zhou, Qin" sort="Zhou, Qin" uniqKey="Zhou Q" first="Qin" last="Zhou">Qin Zhou</name>
</noRegion>
<name sortKey="Cai, Zhen" sort="Cai, Zhen" uniqKey="Cai Z" first="Zhen" last="Cai">Zhen Cai</name>
<name sortKey="Dong, Jiachen" sort="Dong, Jiachen" uniqKey="Dong J" first="Jiachen" last="Dong">Jiachen Dong</name>
<name sortKey="Gu, Xiaoyu" sort="Gu, Xiaoyu" uniqKey="Gu X" first="Xiaoyu" last="Gu">Xiaoyu Gu</name>
<name sortKey="He, Dongmei" sort="He, Dongmei" uniqKey="He D" first="Dongmei" last="He">Dongmei He</name>
<name sortKey="Xu, Ling" sort="Xu, Ling" uniqKey="Xu L" first="Ling" last="Xu">Ling Xu</name>
<name sortKey="Xu, Ling" sort="Xu, Ling" uniqKey="Xu L" first="Ling" last="Xu">Ling Xu</name>
<name sortKey="Yang, Chi" sort="Yang, Chi" uniqKey="Yang C" first="Chi" last="Yang">Chi Yang</name>
<name sortKey="Zheng, Jiawei" sort="Zheng, Jiawei" uniqKey="Zheng J" first="Jiawei" last="Zheng">Jiawei Zheng</name>
<name sortKey="Zhu, Chao" sort="Zhu, Chao" uniqKey="Zhu C" first="Chao" last="Zhu">Chao Zhu</name>
</country>
</tree>
</affiliations>
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