TRPM2 Immunoreactivity Is Increased in Fibroblasts, but not Nerves, of Symptomatic Human Dental Pulp

Rowland, Kevin; Kanive, Courtney B.; Wells, Jason E.; Hatton, John F.

doi:10.1016/j.joen.2006.11.020

Cited by 16 publications

(18 citation statements)

References 30 publications

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“…A difference in immunofluorescence intensity between sections from normal and painful samples that have been processed and stained the same allows an assessment of the biological condition on relative changes in protein expression (17). Even though the immunofluorescence intensity analysis performed in our study did not find a significant difference between normal and painful samples, this method of image analysis has broad applications and has been used by others in human dental pulp studies (18).…”

Section: Discussionmentioning

confidence: 53%

“…Even so, the TRP's represent an important class of receptors involved in peripheral pain mechanisms. For example, an increased expression of TRPM2 was recently identified within nonneuronal cells in the painful human dental pulp (18). This finding suggests that the role of TRP's in pain mechanisms may expand beyond their neuronal expressions.…”

Section: Discussionmentioning

confidence: 95%

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TRPM8 Axonal Expression is Decreased in Painful Human Teeth with Irreversible Pulpitis and Cold Hyperalgesia

Alvarado¹,

Perry²,

Hargreaves³

et al. 2007

Journal of Endodontics

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Pulpitis pain may be triggered by a cold stimulus, yet the cellular mechanisms responsible for this phenomenon are largely unknown. One possible mechanism involves the direct activation of coldresponsive thermoreceptors. The purpose of this study was to evaluate the possible role of the TRPM8 thermoreceptor in cold-mediated noxious pulpal pain mechanisms by comparing expression patterns in pulpal nerves from healthy control molars to cold-sensitive painful molars with irreversible pulpitis. Samples were identically processed with the indirect immunofluorescence method and images obtained with confocal microscopy. The immunofluorescence intensity and area occupied by TRPM8 within N52/PGP9.5 identified nerve fibers were quantified. Results showed that relative to normal samples, TRPM8 nerve area expression was significantly less in the cold-sensitive painful samples (34.9% vs. 8%, p<0.03), but with no significant difference in immunofluorescence intensity between the two groups. These results suggest that TRPM8 is most likely not involved in coldmediated noxious pulpal pain mechanisms.

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Section: Discussionmentioning

confidence: 53%

Section: Discussionmentioning

confidence: 95%

TRPM8 Axonal Expression is Decreased in Painful Human Teeth with Irreversible Pulpitis and Cold Hyperalgesia

Alvarado¹,

Perry²,

Hargreaves³

et al. 2007

Journal of Endodontics

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show abstract

“…However, fibroblasts expressing TRPM2 channels have been so far reported only in the symptomatic dental pulp (43). Thus, our study may be the first report of TRPM2 in rat cardiac fibroblasts.…”

Section: Discussionmentioning

confidence: 58%

Hypoxic Stress Induces Transient Receptor Potential Melastatin 2 (TRPM2) Channel Expression in Adult Rat Cardiac Fibroblasts

2012

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Abstract. When cardiac tissue is exposed to hypoxia, myocytes are damaged, while fibroblasts are activated. However, it is unknown what changes are induced by hypoxia in cardiac fibroblasts. In this study, using the whole cell patch-clamp technique, we investigated the effect of hypoxia on membrane currents in fibroblasts primarily cultured from adult rat hearts. Cardiac fibroblasts were incubated for 24 h under normoxic or hypoxic conditions using Anaeropack. Hypoxia increased a current which reversed at around −20 mV in the cardiac fibroblasts. This current was inhibited by clotrimazole, which is an inhibitor of transient receptor potential melastatin 2 (TRPM2) channel and intermediate-conductance Ca 2+ -activated K + channel (KCa3.1). ADP ribose in the pipette solution enhanced this current. Quantitative RT-PCR revealed that mRNA of TRPM2, but not that of KCa3.1, was increased by hypoxia. RNA interference of TRPM2 prevented the development of the hypoxia-induced current. H 2 O 2 , an activator of TRPM2 channel, induced a higher [Ca 2+ ] i elevation in hypoxia-exposed cardiac fibroblasts than that in normoxia-exposed cells. We conclude that hypoxia induces TRPM2 channel expression in adult rat cardiac fibroblasts.

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“…It has been hypothesized that TRPM2 channel expression is up-regulated in pulp tissue of symptomatic teeth with signs of irreversible pulpitis. It has been demonstrated that during acute pulpitis, TRPM2 expression is increased in cells such as fibroblasts, controlling the release of inflammation mediators (33). These mediators could also be released from other cells, including AAMø CD163ϩ.…”

Section: Discussionmentioning

confidence: 99%

Calcitonin Gene-related Peptide Receptor Expression in Alternatively Activated Monocytes/Macrophages During Irreversible Pulpitis

Caviedes-Bucheli

Moreno

López

et al. 2008

Journal of Endodontics

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TRPM2 Immunoreactivity Is Increased in Fibroblasts, but not Nerves, of Symptomatic Human Dental Pulp

Cited by 16 publications

References 30 publications

TRPM8 Axonal Expression is Decreased in Painful Human Teeth with Irreversible Pulpitis and Cold Hyperalgesia

TRPM8 Axonal Expression is Decreased in Painful Human Teeth with Irreversible Pulpitis and Cold Hyperalgesia

Hypoxic Stress Induces Transient Receptor Potential Melastatin 2 (TRPM2) Channel Expression in Adult Rat Cardiac Fibroblasts

Calcitonin Gene-related Peptide Receptor Expression in Alternatively Activated Monocytes/Macrophages During Irreversible Pulpitis

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