IADR Abstract Archives
Cdk5: a new player implicated in dental pain
Objectives: The cellular and molecular mechanisms involved in tooth pain are not totally understand. Currently, odontoblast theory as a noxious sensor cells is getting high relevance . We reported earlier that Cdk5, a key kinase implicates in orofacial pain, is upregulated by TGF-β1 in odontoblast-like cells, suggesting its possible role in tooth pain. In this study, our aim was to evaluate the expression and regulation of Cdk5 and its activator p35 by inflammatory mediators in both mouse dental cells and trigeminal neurons, and human teeth samples.
Methods: By western blot and immunohistochemical analysis, we evaluated the effect of TNF-α and LPS treatments over Cdk5 and p35 protein expression both in primary cultures of mouse dental cells and in trigeminal sensory neurons. Moreover, by immunofluorescence we analyzed Cdk5-mediated TRPV1 phosphorylation (p-T407-TRPV1), an essential receptor-channel involved in pain signaling and a known Cdk5 substrate.
Results: TNF-α and LPS treatments significantly increased expression of Cdk5 and p35 proteins, and p-T407-TRPV1 levels both in mouse dental cells and in trigeminal sensory neurons. Furthermore, by immunofluorescence we found for the first time that Cdk5, p35 and p-T407-TRPV1 were immunodetected in dentin-pulp complex from human teeth sections.
Conclusions: Our results demonstrate that inflammatory mediators as TNF-α and LPS increase protein expression of Cdk5/p35 and Cdk5-mediated TRPV1 phosphorylation in odontoblast cells and trigeminal sensory neurons, suggesting that Cdk5 contributes to peripheral sensitization during tooth pain.
Neurology
Methods: By western blot and immunohistochemical analysis, we evaluated the effect of TNF-α and LPS treatments over Cdk5 and p35 protein expression both in primary cultures of mouse dental cells and in trigeminal sensory neurons. Moreover, by immunofluorescence we analyzed Cdk5-mediated TRPV1 phosphorylation (p-T407-TRPV1), an essential receptor-channel involved in pain signaling and a known Cdk5 substrate.
Results: TNF-α and LPS treatments significantly increased expression of Cdk5 and p35 proteins, and p-T407-TRPV1 levels both in mouse dental cells and in trigeminal sensory neurons. Furthermore, by immunofluorescence we found for the first time that Cdk5, p35 and p-T407-TRPV1 were immunodetected in dentin-pulp complex from human teeth sections.
Conclusions: Our results demonstrate that inflammatory mediators as TNF-α and LPS increase protein expression of Cdk5/p35 and Cdk5-mediated TRPV1 phosphorylation in odontoblast cells and trigeminal sensory neurons, suggesting that Cdk5 contributes to peripheral sensitization during tooth pain.
Neurology