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NF-B Activation in Human Dental Pulp Stem Cells by TNF and LPS

J. Chang^1,, C. Zhang^2,, N. Tani-Ishii³, S. Shi⁴ and C.-Y. Wang^1,*

¹ Laboratory of Molecular Signaling and Apoptosis, Department of Biologic and Materials Sciences, School of Dentistry, University of Michigan, 1011 N. University Ave., Ann Arbor, MI 48109-1078, USA;
² School of Stomatology, Peking University Health Science Center, Beijing, China;
³ Division of Operative Dentistry and Endodontics, Department of Oral Medicine, Kanagawa Dental College, Kanagawa, Japan; and
⁴ Section of Oral Biology, Craniofacial and Skeletal Diseases Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA;

Correspondence: ^* corresponding author, cunywang{at}umich.edu

Post-natal human dental pulp stem cells (DPSCs) represent a unique precursor population in the dental pulp, which has multipotential and can regenerate a dentin/pulp-like structure. Because the dental pulp is frequently infected by oral bacteria due to dental decay, in this study, we examined whether lipopolysaccharide (LPS) and tumor necrosis factor (TNF) activated the immunologic transcription factor nuclear factor kappa B (NF-B) in DPSCs. We found that both TNF and LPS activated the I-kappa B kinase complex (IKK) in DPSCs to induce the phosphorylation and degradation of IB, resulting in the nuclear translocation of NF-B. Consistently, both TNF and LPS rapidly induced the expression of the NF-B-dependent gene interleukin-8 (IL-8). However, unlike in monocytes, we found that LPS could not induce the phosphorylation of the NF-B active subunit p65 in DPSCs. In summary, our studies suggest that DPSCs may be involved in immune responses during pulpal infection through activating NF-B.

Key Words: NF-B • dental pulp stem cells • tumor necrosis factor • LPS • inflammation.

Journal of Dental Research, Vol. 84, No. 11, 994-998 (2005)
DOI: 10.1177/154405910508401105


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