ArticleMolecular pain2013
TGF-β1 sensitizes TRPV1 through Cdk5 signaling in odontoblast-like cells.
Article in Molecular pain, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 28 citations in OpenAlex.
- Histatin-1 promotes the expression of markers associated with odontoblastic differentiation in the dental pulp and apical papilla.Scientific reports · 2026Article
- Serum Biomarkers of Nociceptive and Neuropathic Pain in Chronic Pancreatitis.The journal of pain · 2023Observational
- Neuronally expressed PDL1, not PD1, suppresses acute nociception.Brain, behavior, and immunity · 2022Article
- Gene expression profiling on effect of aspirin on osteogenic differentiation of periodontal ligament stem cells.BDJ open · 2021Article
- Th2 Modulation of Transient Receptor Potential Channels: An Unmet Therapeutic Intervention for Atopic Dermatitis.Frontiers in immunology · 2021Review
- The Mysteries of Capsaicin-Sensitive Afferents.Frontiers in physiology · 2020Review
- Amino acid sequence conservation of the algesic fragment of myelin basic protein is required for its interaction with CDK5 and function in pain.The FEBS journal · 2018Article
- TNF-α Increases Production of Reactive Oxygen Species through Cdk5 Activation in Nociceptive Neurons.Frontiers in physiology · 2018Article
- Transient Receptor Potential Vanilloid 1 Expression Mediates Capsaicin-Induced Cell Death.Frontiers in physiology · 2018Article
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- Acute Effects of Transforming Growth Factor-β1 on Neuronal Excitability and Involvement in the Pain of Rats with Chronic Pancreatitis.Journal of neurogastroenterology and motility · 2016Article
- TRPV1 function is modulated by Cdk5-mediated phosphorylation: insights into the molecular mechanism of nociception.Scientific reports · 2016Article
- Sigma-1 receptor regulates Tau phosphorylation and axon extension by shaping p35 turnover via myristic acid.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Prenatal stress down-regulates Reelin expression by methylation of its promoter and induces adult behavioral impairments in rats.PloS one · 2015Article
- The role(s) of cytokines/chemokines in urinary bladder inflammation and dysfunction.BioMed research international · 2014Review
- TRPV1 potentiates TGFβ-induction of corneal myofibroblast development through an oxidative stress-mediated p38-SMAD2 signaling loop.PloS one · 2013Article
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7 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundOdontoblasts are specialized cells that form dentin and they are believed to be sensors for tooth pain. Transforming growth factor-β1 (TGF-β1), a pro-inflammatory cytokine expressed early in odontoblasts, plays an important role in the immune response during tooth inflammation and infection. TGF-β1 is also known to participate in pain signaling by regulating cyclin-dependent kinase 5 (Cdk5) in nociceptive neurons of the trigeminal and dorsal root ganglia. However, the precise role of TGF-β1 in tooth pain signaling is not well characterized. The aim of our present study was to determine whether or not in odontoblasts Cdk5 is functionally active, if it is regulated by TGF-β1, and if it affects the downstream pain receptor, transient receptor potential vanilloid-1 (TRPV1).
resultsWe first determined that Cdk5 and p35 are indeed expressed in an odontoblast-enriched primary preparation from murine teeth. For the subsequent analysis, we used an odontoblast-like cell line (MDPC-23) and found that Cdk5 is functionally active in these cells and its kinase activity is upregulated during cell differentiation. We found that TGF-β1 treatment potentiated Cdk5 kinase activity in undifferentiated MDPC-23 cells. SB431542, a specific inhibitor of TGF-β1 receptor 1 (Tgfbr1), when co-administered with TGF-β1, blocked the induction of Cdk5 activity. TGF-β1 treatment also activated the ERK1/2 signaling pathway, causing an increase in early growth response-1 (Egr-1), a transcription factor that induces p35 expression. In MDPC-23 cells transfected with TRPV1, Cdk5-mediated phosphorylation of TRPV1 at threonine-407 was significantly increased after TGF-β1 treatment. In contrast, SB431542 co-treatment blocked TRPV1 phosphorylation. Moreover, TGF-β1 treatment enhanced both proton- and capsaicin-induced Ca²⁺ influx in TRPV1-expressing MDPC-23 cells, while co-treatment with either SB431542 or roscovitine blocked this effect.
conclusionsCdk5 and p35 are expressed in a murine odontoblast-enriched primary preparation of cells from teeth. Cdk5 is also functionally active in odontoblast-like MDPC-23 cells. TGF-β1 sensitizes TRPV1 through Cdk5 signaling in MDPC-23 cells, suggesting the direct involvement of odontoblasts and Cdk5 in dental nociceptive pain transduction.
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