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NF‐κB inhibitor MG132 enhances differentiation and collagen expression of dental pulp stem cells (732.1)
Author(s) -
Saffarian Tousi Hozhabri Neda,
Kim Harry,
Varanasi Venu
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.732.1
Subject(s) - dental pulp stem cells , stem cell , pulp (tooth) , dentin sialophosphoprotein , chemistry , osteocalcin , microbiology and biotechnology , biology , alkaline phosphatase , pathology , medicine , odontoblast , biochemistry , enzyme
Inflammatory response in the dental pulp is mediated by interleukin‐1β and tumor necrosis factor‐α, which may alter collagen matrix formation by dental pulp stem cells and lead to a delay or poor healing of the dental pulp. We hypothesized that these inflammatory cytokines inhibit dental pulp stem cell collagen production by activating the transcription factor nuclear factor ‐ κB. The purpose of this study is to determine the role of nuclear factor ‐ κB signaling during odontoblastic differentiation of human dental pulp stem cells and collagen synthesis under inflammatory culture conditions. Data for the study were obtained by qRT‐PCR and Picrosirius staining for gene expression and collagen matrix staining, respectively. Scanning electron microscopy was used for generating high‐resolution images of the samples. Results showed a significant increase in nuclear factor ‐ κB gene expression by interleukin‐1β and tumor necrosis factor‐α, and this was inhibited in a dose‐dependent manner by a nuclear factor ‐ κB inhibitor (MG132). Interestingly, dental pulp stem cells exposed to inflammatory conditions resulted in a significant increase in collagen (I)‐α1 gene expression, which was further enhanced in the presence of the inhibitor. This correlated with collagen matrix staining. Nuclear factor ‐ κB inhibition also enhanced the gene expression of the odontoblastic marker dentin sialophosphoprotein and demonstrated an odonotblastic cell morphology for the promotion of an odontogenic lineage during inflammation. Conversely, inhibition of NF‐kB in the absence of inflammation resulted in an increase in the gene expression of osteogenic markers (runx2, osteocalcin). In conclusion, controlling inflammatory signaling in DPSCs by reducing the activity of NF‐kB enhances odontoblastic differentiation and collagen matrix formation, potentially stimulating pulp and dentin healing. Grant Funding Source : NIH grants #A107380, #1K25DE018230‐01, #5P30DE020742‐02