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.Research output: Contribution to journal › Article › peer-review
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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 -