LPS promote the odontoblastic differentiation of human dental pulp stem cells via MAPK signaling pathway

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LPS promote the odontoblastic differentiation of human dental pulp stem cells via MAPK signaling pathway. / He, Wenxi; Wang, Zhihua; Luo, Zhirong; Yu, Qing; Jiang, Yong; Zhang, Yaqing; Zhou, Zeyuan; Smith, Anthony J; Cooper, Paul.

In: Journal of Cellular Physiology, Vol. 230, No. 3, 03.2015, p. 554-61.

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He, Wenxi ; Wang, Zhihua ; Luo, Zhirong ; Yu, Qing ; Jiang, Yong ; Zhang, Yaqing ; Zhou, Zeyuan ; Smith, Anthony J ; Cooper, Paul. / LPS promote the odontoblastic differentiation of human dental pulp stem cells via MAPK signaling pathway. In: Journal of Cellular Physiology. 2015 ; Vol. 230, No. 3. pp. 554-61.

Bibtex

@article{8721a157c46040bd8058a9dd62b679e0,
title = "LPS promote the odontoblastic differentiation of human dental pulp stem cells via MAPK signaling pathway",
abstract = "Human dental pulp stem cells (hDPSCs) show significant potential for exploitation in novel regeneration strategies, although lack of understanding of their responses to bacterial challenge constrains their application. The present study aimed to investigate whether lipopolysaccharide (LPS), the major pathogenic factor of Gram-negative bacteria, regulates the differentiation of hDPSCs and which intracellular signaling pathways may be involved. LPS treatment significantly promoted the differentiation of hDPSCs demonstrable by increased mineralized nodule formation and mRNA expression of several odontoblastic markers in a dose-dependent manner. While inhibition of TLR4, p38, and ERK signaling markedly antagonized LPS-mediated differentiation of hDPSCs. The inhibition of JNK and NF-κB signaling had no detectable effect on LPS activation of hDPSCs. LPS stimulation resulted in phosphorylation of NF-κB p65, IκB-α, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) in DPSCs in a time-dependent manner, which was markedly suppressed by their specific inhibitors, respectively. Data demonstrated that LPS promoted odontoblastic differentiation of hDPSCs via TLR4, ERK, and P38 MAPK signaling pathways, but not NF-κB signaling.",
keywords = "Cell Differentiation, Dental Pulp, Humans, Lipopolysaccharides, MAP Kinase Signaling System, NF-kappa B, Odontoblasts, Stem Cells, Toll-Like Receptor 4, Journal Article, Research Support, Non-U.S. Gov't",
author = "Wenxi He and Zhihua Wang and Zhirong Luo and Qing Yu and Yong Jiang and Yaqing Zhang and Zeyuan Zhou and Smith, {Anthony J} and Paul Cooper",
note = "{\textcopyright} 2014 Wiley Periodicals, Inc., A Wiley Company.",
year = "2015",
month = mar,
doi = "10.1002/jcp.24732",
language = "English",
volume = "230",
pages = "554--61",
journal = "Journal of Cellular Physiology",
issn = "0021-9541",
publisher = "Wiley",
number = "3",

}

RIS

TY - JOUR

T1 - LPS promote the odontoblastic differentiation of human dental pulp stem cells via MAPK signaling pathway

AU - He, Wenxi

AU - Wang, Zhihua

AU - Luo, Zhirong

AU - Yu, Qing

AU - Jiang, Yong

AU - Zhang, Yaqing

AU - Zhou, Zeyuan

AU - Smith, Anthony J

AU - Cooper, Paul

N1 - © 2014 Wiley Periodicals, Inc., A Wiley Company.

PY - 2015/3

Y1 - 2015/3

N2 - Human dental pulp stem cells (hDPSCs) show significant potential for exploitation in novel regeneration strategies, although lack of understanding of their responses to bacterial challenge constrains their application. The present study aimed to investigate whether lipopolysaccharide (LPS), the major pathogenic factor of Gram-negative bacteria, regulates the differentiation of hDPSCs and which intracellular signaling pathways may be involved. LPS treatment significantly promoted the differentiation of hDPSCs demonstrable by increased mineralized nodule formation and mRNA expression of several odontoblastic markers in a dose-dependent manner. While inhibition of TLR4, p38, and ERK signaling markedly antagonized LPS-mediated differentiation of hDPSCs. The inhibition of JNK and NF-κB signaling had no detectable effect on LPS activation of hDPSCs. LPS stimulation resulted in phosphorylation of NF-κB p65, IκB-α, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) in DPSCs in a time-dependent manner, which was markedly suppressed by their specific inhibitors, respectively. Data demonstrated that LPS promoted odontoblastic differentiation of hDPSCs via TLR4, ERK, and P38 MAPK signaling pathways, but not NF-κB signaling.

AB - Human dental pulp stem cells (hDPSCs) show significant potential for exploitation in novel regeneration strategies, although lack of understanding of their responses to bacterial challenge constrains their application. The present study aimed to investigate whether lipopolysaccharide (LPS), the major pathogenic factor of Gram-negative bacteria, regulates the differentiation of hDPSCs and which intracellular signaling pathways may be involved. LPS treatment significantly promoted the differentiation of hDPSCs demonstrable by increased mineralized nodule formation and mRNA expression of several odontoblastic markers in a dose-dependent manner. While inhibition of TLR4, p38, and ERK signaling markedly antagonized LPS-mediated differentiation of hDPSCs. The inhibition of JNK and NF-κB signaling had no detectable effect on LPS activation of hDPSCs. LPS stimulation resulted in phosphorylation of NF-κB p65, IκB-α, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) in DPSCs in a time-dependent manner, which was markedly suppressed by their specific inhibitors, respectively. Data demonstrated that LPS promoted odontoblastic differentiation of hDPSCs via TLR4, ERK, and P38 MAPK signaling pathways, but not NF-κB signaling.

KW - Cell Differentiation

KW - Dental Pulp

KW - Humans

KW - Lipopolysaccharides

KW - MAP Kinase Signaling System

KW - NF-kappa B

KW - Odontoblasts

KW - Stem Cells

KW - Toll-Like Receptor 4

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1002/jcp.24732

DO - 10.1002/jcp.24732

M3 - Article

C2 - 25104580

VL - 230

SP - 554

EP - 561

JO - Journal of Cellular Physiology

JF - Journal of Cellular Physiology

SN - 0021-9541

IS - 3

ER -