TNF-α Promotes an Odontoblastic Phenotype in Dental Pulp Cells

Paula-Silva, Francisco Wanderley Garcia; Ghosh, Abhijit; Silva, L.A.B.; Kapila, Yvonne L.

doi:10.1177/0022034509334070

Cited by 141 publications

(82 citation statements)

References 36 publications

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“…8D). Western blotting confirmed expression of DSP, an odontogenic differentiation marker (42), in NHEK/⌬Np63␣-M and DPSC, and absence of the protein expression in NHEK and NHEK/Snail (Fig. 8E).…”

Section: Transduction Of ⌬Np63␣mentioning

confidence: 75%

ΔNp63α Protein Triggers Epithelial-Mesenchymal Transition and Confers Stem Cell Properties in Normal Human Keratinocytes

Kim

Shin

et al. 2011

Journal of Biological Chemistry

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Background: ⌬Np63␣ is an isoform of p63 that is predominantly expressed in normal epidermis. Results: Retroviral transduction of ⌬Np63␣ into rapidly proliferating primary human epidermal keratinocytes led to epithelialmesenchymal transition (EMT) and acquisition of stemlike properties. Conclusion: ⌬Np63␣ regulates EMT in primary human keratinocytes in a TGF-␤-dependent manner. Significance: Altering p63 level in NHEK may be a novel method to generate "induced mesenchymal stem cells" with multipotent capacity.

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Section: Transduction Of ⌬Np63␣mentioning

confidence: 75%

ΔNp63α Protein Triggers Epithelial-Mesenchymal Transition and Confers Stem Cell Properties in Normal Human Keratinocytes

Kim

Shin

et al. 2011

Journal of Biological Chemistry

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“…In a first approach, we demonstrated that the recombinant C-DMP1 polypeptide, mimicking the limited cleavage products obtained by MMP-2, had a profound effect on the differentiation of dental pulp stem/progenitor cells, not observed with the N- polypeptide. Differentiation into putative odontoblast was revealed by the rapid organization of most of the cells into clusters and the increased expression of odontoblast differentiation markers, namely DMP1 and DSPP (Hao et al, 2009, Hao et al , 2004, Paula-Silva et al , 2009). However, as DPSCs are a heterogeneous cell population, further investigations using sorted pulp stem cells will allow us to investigate the mechanism induced by DMP1 derived peptides on pulp cell differentiation.…”

Section: Discussionmentioning

confidence: 99%

MMP2-cleavage of DMP1 generates a bioactive peptide promoting differentiation of dental pulp stem/progenitor cell

Chaussain

Eapen

Huet

et al. 2009

eCM

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Dentin Matrix Protein 1 (DMP1) plays a regulatory role in dentin mineralization and can also function as a signaling molecule. MMP-2 (matrix metalloproteinase-2) is a predominant protease in the dentin matrix that plays a prominent role in tooth formation and a potential role during the carious process. The possibility that MMP-2 can cleave DMP1 to release biologically active peptides was investigated in this study. DMP1, both in the recombinant form and in its native state within the dentin matrix, was shown to be a substrate for MMP-2. Proteolytic processing of DMP1 by MMP-2 produced two major peptides, one that contains the C-terminal region of the protein known to carry both the ASARM (aspartic acid and serine rich domain) domain involved in biomineralization and the DNA binding site of DMP1. In vitro experiments with recombinant N-and C-terminal polypeptides mimicking the MMP-2 cleavage products of DMP1 demonstrated an effect of the C-polypeptide on the differentiation of dental pulp stem/progenitor cells to a putative odontoblast phenotype. In vivo implantation of this peptide in a rat injured pulp model induced a rapid formation of a homogeneous dentin bridge covered by a palisade of orientated cells expressing dentin sialoprotein (DSP) and DMP1, attesting an efficient repair process. These data suggest that a peptide generated through the proteolytic processing of DMP1 by MMP-2 can regulate the differentiation of mesenchymal cells during dentinogenesis and thus sustain reparative dentin formation in pathological situations such as carious decay. In addition, these data open a new therapeutic possibility of using this peptide to regenerate dentin after an injury.

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“…83 In the absence of dexamethasone, treatment of osteoprogenitors with TNF-a resulted in dose-dependent increases in ALP activity and mineralized matrix deposition, which are, respectively, early and late markers of osteogenesis. 12,83,[86][87][88] In contrast, when added to dexamethasonecontaining osteogenic medium, TNF-a had the opposite effect on MSCs. 89,90 The pro-regenerative effects of TNF-a seen in dexamethasone-free in vitro MSC cultures were recently confirmed in vivo through repeated injections of TNF-a into a fracture healing model.…”

Section: Tnf-amentioning

confidence: 99%