Protease-activated receptor 2 expression in trigeminal neurons innervating the rat nasal mucosa

Dinh, Q. Thai; Cryer, Annette; Dinh, S. Tran; Trevisani, Marcello; Georgiewa, Petra; Chung, Fan; Geppetti, Pierangelo; Heppt, Werner J.; Klapp, Burghard F.; Fischer, Axel

doi:10.1016/j.npep.2005.07.003

Cited by 24 publications

(16 citation statements)

References 39 publications

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“…In trigeminal ganglion neurons, PAR 2 receptors are found on neurons that do not express tachykinins (Dinh et al, 2005). This and the present observation that PAR 2 depolarized large cells suggest that it is capable of affecting neurons that do not express tachykinins.…”

Section: Discussionsupporting

confidence: 66%

Intrathecal Administration of Proteinase-Activated Receptor-2 Agonists Produces Hyperalgesia by Exciting the Cell Bodies of Primary Sensory Neurons

Alier¹,

Endicott²,

Stemkowski³

et al. 2007

J Pharmacol Exp Ther

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Proteinase-activated receptors (PARs) are a family of G-protein-coupled receptors that are activated by endogenous serine proteinases that cleave the N-terminal domain of the receptor unmasking a "tethered ligand" sequence. Trypsin and other agonists at PAR(2) act on peripheral nerves to augment the transfer of nociceptive information. We tested whether PAR(2) agonists also exert a spinal pronociceptive effect by i.t. administering the selective ligand, Ser-Leu-Ile-Gly-Arg-Leu-NH(2) (SLI-GRL). This produced thermal and mechanical hyperalgesia in rats and mice and augmented mechanical and thermal hyperalgesia seen in the formalin inflammatory pain test. Effects of SLIGRL were abrogated in PAR(2)-deficient mice and were not seen with the inactive control peptide, Leu-Arg-Gly-Ile-Leu-Ser-NH(2). Surprisingly, electrophysiological studies, using whole-cell recording from rat substantia gelatinosa neurons, failed to demonstrate an increase in excitatory transmission or neuronal excitability following treatment with SLIGRL or trypsin. In fact, the actions of trypsin were consistent with a decrease in dorsal horn excitability. SLIGRL and trypsin did, however, depolarize and increase the excitability of large, medium and small primary afferent, dorsal root ganglion neurons. The effects were associated with an increase in conductance at hyperpolarized potentials and a decrease in conductance at depolarized potentials. PAR(2)-like immunoreactivity was found in DRG but not in spinal dorsal horn. These results suggest that activation of DRG neuron cell bodies may account for the pronociceptive actions of i.t. applied PAR(2) agonists. They also imply that pathophysiological release of PAR(2)-activating proteases in the vicinity of DRG neurons may produce profound effects on nociceptive processing in vivo.

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Section: Discussionsupporting

confidence: 66%

Intrathecal Administration of Proteinase-Activated Receptor-2 Agonists Produces Hyperalgesia by Exciting the Cell Bodies of Primary Sensory Neurons

Alier¹,

Endicott²,

Stemkowski³

et al. 2007

J Pharmacol Exp Ther

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“…The extend co‐localization of PAR 2 and other pro‐inflammatory neuropeptides like tachykinins and CGRP in sensory neurons indicate a role of PAR 2 in neurogenic airway inflammation [41]. Moreover, PAR 2 has been shown to express on sensory neurons [42]. Activation of PAR 2 on sensory nerves was able to mediate neurogenic inflammation via tachykininergic pathway [7].…”

Section: Discussionmentioning

confidence: 99%

Gene and protein expression of protease‐activated receptor 2 in structural and inflammatory cells in the nasal mucosa in seasonal allergic rhinitis

Dinh

Cryer

Trevisani

et al. 2006

Clin Experimental Allergy

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“…Recently, the maturation and differentiation of DC have been described to be modulated by many cytokines of immune cells as well as neuropeptides such as the calcitonin gene-related peptide (CGRP) released by airway sensory nerve fibers [8,9,10,11,12,13]. …”

Section: Introductionmentioning

confidence: 99%

Steroid Treatment Reduces Allergic Airway Inflammation and Does Not Alter the Increased Numbers of Dendritic Cells and Calcitonin Gene-Related Peptide-Expressing Neurons in Airway Sensory Ganglia

Funck²,

Wronski³

et al. 2015

Neuroimmunomodulation

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Objectives: Our previous data demonstrated that allergic airway inflammation induces migration of dendritic cells (DC) into airway sensory jugular and nodose ganglia (jugular-nodose ganglion complex; JNC). Here we investigated the effects of steroid treatment regarding the expression and migration of DC and calcitonin gene-related peptide (CGRP)-immunoreactive neurons of vagal sensory ganglia during allergic airway inflammation. Methods: A house dust mite (HDM) model for allergic airway inflammation was used. The mice received 0.3 mg fluticasone propionate per kilogram of body weight in the last 9 days. JNC slices were analyzed on MHC II, the neuronal marker PGP9.5, and the neuropeptide CGRP. Results: Allergic airway inflammation increased the numbers of DC and CGRP-expressing neurons in the JNCsignificantly in comparison to the controls (DC/neurons: HDM 44.58 ± 1.6% vs. saline 33.29 ± 1.6%, p < 0.05; CGRP-positive neurons/total neurons: HDM 30.65 ± 1.9% vs. saline 19.49 ± 2.3%, p < 0.05). Steroid treatmentdid not have any effect on the numbers of DC and CGRP-expressing neurons in the JNC compared to HDM-treated mice. Conclusions: The present findings indicate an important role of DC and CGRP-containing neurons in the pathogenesis of allergic airway inflammation. However, steroid treatment did not have an effect on the population of DC and neurons displaying CGRP in the JNC, whereas steroid treatment was found to suppress allergic airway inflammation.

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Protease-activated receptor 2 expression in trigeminal neurons innervating the rat nasal mucosa

Cited by 24 publications

References 39 publications

Intrathecal Administration of Proteinase-Activated Receptor-2 Agonists Produces Hyperalgesia by Exciting the Cell Bodies of Primary Sensory Neurons

Intrathecal Administration of Proteinase-Activated Receptor-2 Agonists Produces Hyperalgesia by Exciting the Cell Bodies of Primary Sensory Neurons

Gene and protein expression of protease‐activated receptor 2 in structural and inflammatory cells in the nasal mucosa in seasonal allergic rhinitis

Steroid Treatment Reduces Allergic Airway Inflammation and Does Not Alter the Increased Numbers of Dendritic Cells and Calcitonin Gene-Related Peptide-Expressing Neurons in Airway Sensory Ganglia

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