Bone morphogenetic protein 2-induced human dental pulp cell differentiation involves p38 mitogen-activated protein kinase-activated canonical WNT pathway

Both bone morphogenetic protein 2（BMP2） and the wingless-type MMTV integration site（WNT）/p-catenin signalling pathway play important roles in odontoblast differentiation and dentinogenesis.Cross-talk between BMP2 and WNT/p-catenin in osteoblast differentiation and bone formation has been identified....

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Published inInternational journal of oral science Vol. 7; no. 2; pp. 95 - 102
Main Authors Yang, Jing, Ye, Ling, Hui, Tian-Qian, Yang, Dong-Mei, Huang, Ding-Ming, Zhou, Xue-Dong, Mao, Jeremy J, Wang, Cheng-Lin
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.06.2015
Springer Nature B.V
State Key Laboratory of 0ral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China%Center for Craniofacial Regeneration CCR, Columbia University Medical Center, New York, USA
Nature Publishing Group
Subjects
beta Catenin - metabolism
Bone Morphogenetic Protein 2 - physiology
Cell Differentiation - physiology
Dental Pulp - cytology
Dentistry
Humans
MAP Kinase Signaling System
Medicine
Oral and Maxillofacial Surgery
Original
original-article
Orthopedics
p38丝裂原活化蛋白激酶
Surgical Orthopedics
Wnt Proteins - metabolism
Wnt信号通路
β-catenin
成骨细胞分化
牙髓
诱导蛋白
酶激活
骨形态发生蛋白
human dental pulp cells
β-catenin
cell differentiation
bone morphogenetic protein 2
p38
b-catenin
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Abstract Both bone morphogenetic protein 2（BMP2） and the wingless-type MMTV integration site（WNT）/p-catenin signalling pathway play important roles in odontoblast differentiation and dentinogenesis.Cross-talk between BMP2 and WNT/p-catenin in osteoblast differentiation and bone formation has been identified.However,the roles and mechanisms of the canonical WNT pathway in the regulation of BMP2 in dental pulp injury and repair remain largely unknown.Here,we demonstrate that BMP2 promotes the differentiation of human dental pulp cells（HDPCs） by activating WNT/p-catenin signalling,which is further mediated by p38mitogen-activated protein kinase（MAPK） in vitro.BMP2 stimulation upregulated the expression of p-catenin in HDPCs,which was abolished by SB203580 but not by Noggin or LDN193189.Furthermore,BMP2 enhanced cell differentiation,which was not fully inhibited by Noggin or LDN193189.Instead,SB203580 partially blocked BMP2-induced p-catenin expression and cell differentiation.Taken together,these data suggest a possible mechanism by which the elevation of p-catenin resulting from BMP2 stimulation is mediated by the p38 MAPK pathway,which sheds light on the molecular mechanisms of BMP2-mediated pulp reparative dentin formation.
AbstractList Both bone morphogenetic protein 2 (BMP2) and the wingless-type MMTV integration site (WNT)/b-catenin signalling pathway play important roles in odontoblast differentiation and dentinogenesis. Cross-talk between BMP2 and WNT/b-catenin in osteoblast differentiation and bone formation has been identified. However, the roles and mechanisms of the canonical WNT pathway in the regulation of BMP2 in dental pulp injury and repair remain largely unknown. Here, we demonstrate that BMP2 promotes the differentiation of human dental pulp cells (HDPCs) by activating WNT/b-catenin signalling, which is further mediated by p38 mitogen-activated protein kinase (MAPK) in vitro. BMP2 stimulation upregulated the expression of b-catenin in HDPCs, which was abolished by SB203580 but not by Noggin or LDN193189. Furthermore, BMP2 enhanced cell differentiation, which was not fully inhibited by Noggin or LDN193189. Instead, SB203580 partially blocked BMP2-induced b-catenin expression and cell differentiation. Taken together, these data suggest a possible mechanism by which the elevation of b-catenin resulting from BMP2 stimulation is mediated by the p38 MAPK pathway, which sheds light on the molecular mechanisms of BMP2-mediated pulp reparative dentin formation.
Both bone morphogenetic protein 2（BMP2） and the wingless-type MMTV integration site（WNT）/p-catenin signalling pathway play important roles in odontoblast differentiation and dentinogenesis.Cross-talk between BMP2 and WNT/p-catenin in osteoblast differentiation and bone formation has been identified.However,the roles and mechanisms of the canonical WNT pathway in the regulation of BMP2 in dental pulp injury and repair remain largely unknown.Here,we demonstrate that BMP2 promotes the differentiation of human dental pulp cells（HDPCs） by activating WNT/p-catenin signalling,which is further mediated by p38mitogen-activated protein kinase（MAPK） in vitro.BMP2 stimulation upregulated the expression of p-catenin in HDPCs,which was abolished by SB203580 but not by Noggin or LDN193189.Furthermore,BMP2 enhanced cell differentiation,which was not fully inhibited by Noggin or LDN193189.Instead,SB203580 partially blocked BMP2-induced p-catenin expression and cell differentiation.Taken together,these data suggest a possible mechanism by which the elevation of p-catenin resulting from BMP2 stimulation is mediated by the p38 MAPK pathway,which sheds light on the molecular mechanisms of BMP2-mediated pulp reparative dentin formation.
Both bone morphogenetic protein 2 (BMP2) and the wingless-type MMTV integration site (WNT)/β-catenin signalling pathway play important roles in odontoblast differentiation and dentinogenesis. Cross-talk between BMP2 and WNT/β-catenin in osteoblast differentiation and bone formation has been identified. However, the roles and mechanisms of the canonical WNT pathway in the regulation of BMP2 in dental pulp injury and repair remain largely unknown. Here, we demonstrate that BMP2 promotes the differentiation of human dental pulp cells (HDPCs) by activating WNT/β-catenin signalling, which is further mediated by p38 mitogen-activated protein kinase (MAPK) in vitro. BMP2 stimulation upregulated the expression of β-catenin in HDPCs, which was abolished by SB203580 but not by Noggin or LDN193189. Furthermore, BMP2 enhanced cell differentiation, which was not fully inhibited by Noggin or LDN193189. Instead, SB203580 partially blocked BMP2-induced β-catenin expression and cell differentiation. Taken together, these data suggest a possible mechanism by which the elevation of β-catenin resulting from BMP2 stimulation is mediated by the p38 MAPK pathway, which sheds light on the molecular mechanisms of BMP2-mediated pulp reparative dentin formation.
Both bone morphogenetic protein 2 (BMP2) and the wingless-type MMTV integration site (WNT)/β-catenin signalling pathway play important roles in odontoblast differentiation and dentinogenesis. Cross-talk between BMP2 and WNT/β-catenin in osteoblast differentiation and bone formation has been identified. However, the roles and mechanisms of the canonical WNT pathway in the regulation of BMP2 in dental pulp injury and repair remain largely unknown. Here, we demonstrate that BMP2 promotes the differentiation of human dental pulp cells (HDPCs) by activating WNT/β-catenin signalling, which is further mediated by p38 mitogen-activated protein kinase (MAPK) in vitro. BMP2 stimulation upregulated the expression of β-catenin in HDPCs, which was abolished by SB203580 but not by Noggin or LDN193189. Furthermore, BMP2 enhanced cell differentiation, which was not fully inhibited by Noggin or LDN193189. Instead, SB203580 partially blocked BMP2-induced β-catenin expression and cell differentiation. Taken together, these data suggest a possible mechanism by which the elevation of β-catenin resulting from BMP2 stimulation is mediated by the p38 MAPK pathway, which sheds light on the molecular mechanisms of BMP2-mediated pulp reparative dentin formation.Both bone morphogenetic protein 2 (BMP2) and the wingless-type MMTV integration site (WNT)/β-catenin signalling pathway play important roles in odontoblast differentiation and dentinogenesis. Cross-talk between BMP2 and WNT/β-catenin in osteoblast differentiation and bone formation has been identified. However, the roles and mechanisms of the canonical WNT pathway in the regulation of BMP2 in dental pulp injury and repair remain largely unknown. Here, we demonstrate that BMP2 promotes the differentiation of human dental pulp cells (HDPCs) by activating WNT/β-catenin signalling, which is further mediated by p38 mitogen-activated protein kinase (MAPK) in vitro. BMP2 stimulation upregulated the expression of β-catenin in HDPCs, which was abolished by SB203580 but not by Noggin or LDN193189. Furthermore, BMP2 enhanced cell differentiation, which was not fully inhibited by Noggin or LDN193189. Instead, SB203580 partially blocked BMP2-induced β-catenin expression and cell differentiation. Taken together, these data suggest a possible mechanism by which the elevation of β-catenin resulting from BMP2 stimulation is mediated by the p38 MAPK pathway, which sheds light on the molecular mechanisms of BMP2-mediated pulp reparative dentin formation.
Both bone morphogenetic protein 2 (BMP2) and the wingless-type MMTV integration site (WNT)/β-catenin signalling pathway play important roles in odontoblast differentiation and dentinogenesis. Cross-talk between BMP2 and WNT/β-catenin in osteoblast differentiation and bone formation has been identified. However, the roles and mechanisms of the canonical WNT pathway in the regulation of BMP2 in dental pulp injury and repair remain largely unknown. Here, we demonstrate that BMP2 promotes the differentiation of human dental pulp cells (HDPCs) by activating WNT/β-catenin signalling, which is further mediated by p38 mitogen-activated protein kinase (MAPK) in vitro . BMP2 stimulation upregulated the expression of β-catenin in HDPCs, which was abolished by SB203580 but not by Noggin or LDN193189. Furthermore, BMP2 enhanced cell differentiation, which was not fully inhibited by Noggin or LDN193189. Instead, SB203580 partially blocked BMP2-induced β-catenin expression and cell differentiation. Taken together, these data suggest a possible mechanism by which the elevation of β-catenin resulting from BMP2 stimulation is mediated by the p38 MAPK pathway, which sheds light on the molecular mechanisms of BMP2-mediated pulp reparative dentin formation.
Both bone morphogenetic protein 2 (BMP2) and the wingless-type MMTV integration site (WNT)/β-catenin signalling pathway play important roles in odontoblast differentiation and dentinogenesis. Cross-talk between BMP2 and WNT/β-catenin in osteoblast differentiation and bone formation has been identified. However, the roles and mechanisms of the canonical WNT pathway in the regulation of BMP2 in dental pulp injury and repair remain largely unknown. Here, we demonstrate that BMP2 promotes the differentiation of human dental pulp cells (HDPCs) by activating WNT/β-catenin signalling, which is further mediated by p38 mitogen-activated protein kinase (MAPK) in vitro . BMP2 stimulation upregulated the expression of β-catenin in HDPCs, which was abolished by SB203580 but not by Noggin or LDN193189. Furthermore, BMP2 enhanced cell differentiation, which was not fully inhibited by Noggin or LDN193189. Instead, SB203580 partially blocked BMP2-induced β-catenin expression and cell differentiation. Taken together, these data suggest a possible mechanism by which the elevation of β-catenin resulting from BMP2 stimulation is mediated by the p38 MAPK pathway, which sheds light on the molecular mechanisms of BMP2-mediated pulp reparative dentin formation. Dentin: The pathways from pulp Researchers have clarified the molecular interactions that underpin the formation and regeneration of dentin in human teeth. Dentin is the layer of calcified tissue directly beneath the surface enamel of a tooth. It is formed and sustained by the differentiation of cells in the tooth pulp that lies beneath the dentin layer. Chenglin Wang and co-workers at Sichuan University in China, with colleagues at Columbia University, New York, USA, studied human dental pulp cells in vitro . They demonstrated that bone morphogenetic protein 2 (BMP2) promotes the differentiation of pulp cells to form dentin by affecting signaling pathways known to be involved. Identifying the links between the growth factor BMP2, and β -catenin and p38, proteins in these pathways, will improve understanding of dentin formation and repair after injury.
Author Jing Yang Ling Ye Tian-Qian Hui Dong-Mei Yang Ding-Ming Huang Xue-Dong Zhou Jeremy J Mao Cheng-Lin Wang
AuthorAffiliation State Key Laboratory of Oral Diseases, West China Hospital of Stomatolosy, Sichuan University, Chengdu, China Center for Craniofacial Regeneration （CCR）, Columbia University Medical Center, New York, USA
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/26047580$$D View this record in MEDLINE/PubMed
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DocumentTitleAlternate Bone morphogenetic protein 2-induced human dental pulp cell differentiation involves p38 mitogen-activated protein kinase-activated canonical WNT pathway
BMP2-p38 induced differentiation by WNT pathway
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Issue 2
Keywords human dental pulp cells
β-catenin
cell differentiation
bone morphogenetic protein 2
p38
b-catenin
Language English
License This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0
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Notes 51-1707/R
Both bone morphogenetic protein 2（BMP2） and the wingless-type MMTV integration site（WNT）/p-catenin signalling pathway play important roles in odontoblast differentiation and dentinogenesis.Cross-talk between BMP2 and WNT/p-catenin in osteoblast differentiation and bone formation has been identified.However,the roles and mechanisms of the canonical WNT pathway in the regulation of BMP2 in dental pulp injury and repair remain largely unknown.Here,we demonstrate that BMP2 promotes the differentiation of human dental pulp cells（HDPCs） by activating WNT/p-catenin signalling,which is further mediated by p38mitogen-activated protein kinase（MAPK） in vitro.BMP2 stimulation upregulated the expression of p-catenin in HDPCs,which was abolished by SB203580 but not by Noggin or LDN193189.Furthermore,BMP2 enhanced cell differentiation,which was not fully inhibited by Noggin or LDN193189.Instead,SB203580 partially blocked BMP2-induced p-catenin expression and cell differentiation.Taken together,these data suggest a possible mechanism by which the elevation of p-catenin resulting from BMP2 stimulation is mediated by the p38 MAPK pathway,which sheds light on the molecular mechanisms of BMP2-mediated pulp reparative dentin formation.
dental catenin morphogenetic stimulation canonical inhibited blocked repair activating mitogen
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content type line 23
OpenAccessLink http://journals.scholarsportal.info/openUrl.xqy?doi=10.1038/ijos.2015.7
PMID 26047580
PQID 1799853555
PQPubID 2041951
PageCount 8
ParticipantIDs pubmedcentral_primary_oai_pubmedcentral_nih_gov_4817555
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crossref_citationtrail_10_1038_ijos_2015_7
springer_journals_10_1038_ijos_2015_7
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ProviderPackageCode CITATION
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PublicationCentury 2000
PublicationDate 2015-06-01
PublicationDateYYYYMMDD 2015-06-01
PublicationDate_xml – month: 06
  year: 2015
  text: 2015-06-01
  day: 01
PublicationDecade 2010
PublicationPlace London
PublicationPlace_xml – name: London
– name: India
PublicationTitle International journal of oral science
PublicationTitleAbbrev Int J Oral Sci
PublicationTitleAlternate International Journal of Oral Science
PublicationTitle_FL International Journal of Oral Science
PublicationYear 2015
Publisher Nature Publishing Group UK
Springer Nature B.V
State Key Laboratory of 0ral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China%Center for Craniofacial Regeneration CCR, Columbia University Medical Center, New York, USA
Nature Publishing Group
Publisher_xml – name: Nature Publishing Group UK
– name: Springer Nature B.V
– name: State Key Laboratory of 0ral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China%Center for Craniofacial Regeneration CCR, Columbia University Medical Center, New York, USA
– name: Nature Publishing Group
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SSID ssj0068521
Score 2.246002
Snippet Both bone morphogenetic protein 2（BMP2） and the wingless-type MMTV integration site（WNT）/p-catenin signalling pathway play important roles in odontoblast...
Both bone morphogenetic protein 2 (BMP2) and the wingless-type MMTV integration site (WNT)/β-catenin signalling pathway play important roles in odontoblast...
Both bone morphogenetic protein 2 (BMP2) and the wingless-type MMTV integration site (WNT)/b-catenin signalling pathway play important roles in odontoblast...
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StartPage 95
SubjectTerms beta Catenin - metabolism
Bone Morphogenetic Protein 2 - physiology
Cell Differentiation - physiology
Dental Pulp - cytology
Dentistry
Humans
MAP Kinase Signaling System
Medicine
Oral and Maxillofacial Surgery
Original
original-article
Orthopedics
p38丝裂原活化蛋白激酶
Surgical Orthopedics
Wnt Proteins - metabolism
Wnt信号通路
β-catenin
成骨细胞分化
牙髓
诱导蛋白
酶激活
骨形态发生蛋白
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Title Bone morphogenetic protein 2-induced human dental pulp cell differentiation involves p38 mitogen-activated protein kinase-activated canonical WNT pathway
URI http://lib.cqvip.com/qk/89520X/201502/665387912.html
https://link.springer.com/article/10.1038/ijos.2015.7
https://www.ncbi.nlm.nih.gov/pubmed/26047580
https://www.proquest.com/docview/1799853555
https://www.proquest.com/docview/1691597086
https://d.wanfangdata.com.cn/periodical/gjkqkxzz-e201502005
https://pubmed.ncbi.nlm.nih.gov/PMC4817555
Volume 7
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