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Pharmaceuticals
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TRPA1 Receptor as a Potential Therapeutic Target in Pain, Inflammation...
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TRPA1 Receptor as a Potential Therapeutic Target in Pain, Inflammation and Neurodegeneration

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: closed (31 March 2022) | Viewed by 7372

Special Issue Editors

Prof. Erika Pintér

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Guest Editor
Department of Pharmacology and Pharmacotherapy, Medical School University of Pecs, Pecs, Hungary
Interests: pain; inflammation; neuro-immune-pharmacology; neurodegeneration
Prof. Dr. Susan D. Brain

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Guest Editor
School of Cardiovascular & Metabolic Medicine and Sciences, King's College, London, UK
Interests: sensory nerves; vascular inflammation; TRP receptors; CGRP
Special Issues, Collections and Topics in MDPI journals
Dr. Romina Nassini

E-Mail Website
Guest Editor
Department of Health Sciences, Clinical Pharmacology Unit, University of Florence, 50139 Florence, Italy
Interests: neuroscience; pharmacology; ion channel; pain
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The journal Pharmaceuticals is planning to publish a Special Issue covering the topic “TRPA1 Receptor as a Potential Therapeutic Target in Pain, Inflammation and Neurodegeneration”, and I am cordially inviting you to contribute an article to this volume. 

Transient Receptor Potential Ankyrin 1 TRPA1, a member of the TRP superfamily, has unique aspects, particularly considering its wide range of ligands, making it a really promiscuous receptor. TRPA1 behaves as an integrator of endogenous and exogenous activators. TRPA1 can be triggered by endogenous compounds generated during tissue injury and inflammation. Therefore, recent trends in drug development consider TRPA1 as a novel potential drug target for pain killers and anti-inflammatory drug candidates. TRPA1 channels are also expressed in the brain and play a role in neurodegenerative disorders and neuroinflammation. Expression of TRPA1 by somatic and visceral primary sensory neurones is well-known. Several data indicated that TRPA1-mediated events modulate a number of chronic pain conditions associated with tissue injury and inflammation. It is well known that pro-inflammatory and algogenic mediators, released within the injured or inflamed tissue, modulate TRPA1. Expression of non-neuronal TRPA1 has been manifested in several cell types (fibroblasts, epithelial-, smooth muscle cells melanocytes, keratinocytes, oligodendrocytes/Schwann cells) and, therefore, it has been hypothesized as a regulator receptor. Whilst the pro-inflammatory effects of TRPA1 activation are well established, there is emerging evidence for its protective effects. Besides TRPA1 receptors expressed on sensory neurons, the activities of the non-neuronal TRPA1 must not be forgotten. Given its expression in many different types of tissues and cells, and its pleiotropic biological profile, TRPA1 represents an attractive therapeutic target, thus opening new potential strategies for the treatment of a variety of human diseases.   

The purpose of this Special Issue is to host research and review papers providing evidence that TRPA1 receptor could be considered as a promising drug target in the treatment of pain, inflammation or degenerative disorders.

Areas of interest include, but are not limited to:

  • Identification of TRPA1 as a potential drug target
  • Design of novel TRPA1 specific ligands
  • The role of TRPA1 in pain and inflammation
  • Expression pattern and function of TRPA1 in the CNS
  • The role of TRPA1 in  neurodegenerationTRPA1-mediated effects of sulfide compoundsTRPA1 receptor in skin diseases.
  • The role of TRPA1 as a regulatory molecule.

Prof. Erika Pintér
Prof. Susan D. Brain
Dr. Romina Nassini
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pharmaceuticals is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • TRPA1 receptor
  • pain
  • inflammation
  • neurodegeneration
  • drug development
  • CNS
  • skin
  • polysulfides

Published Papers (2 papers)

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Research

13 pages, 1626 KiB  
Article
Transient Receptor Potential Ankyrin-1 (TRPA1) Block Protects against Loss of White Matter Function during Ischaemia in the Mouse Optic Nerve
by Wendy Lajoso, Grace Flower, Vincenzo Giacco, Anjuli Kaul, Circe La Mache, Andra Brăban, Angela Roxas and Nicola B. Hamilton
Pharmaceuticals 2021, 14(9), 909; https://doi.org/10.3390/ph14090909 - 09 Sep 2021
Cited by 6 | Viewed by 2918
Abstract
Oligodendrocytes produce myelin, which provides insulation to axons and speeds up neuronal transmission. In ischaemic conditions, myelin is damaged, resulting in mental and physical disabilities. Recent evidence suggests that oligodendrocyte damage during ischaemia can be mediated by Transient Receptor Potential Ankyrin-1 (TRPA1), whose [...] Read more.
Oligodendrocytes produce myelin, which provides insulation to axons and speeds up neuronal transmission. In ischaemic conditions, myelin is damaged, resulting in mental and physical disabilities. Recent evidence suggests that oligodendrocyte damage during ischaemia can be mediated by Transient Receptor Potential Ankyrin-1 (TRPA1), whose activation raises intracellular Ca2+ concentrations and damages compact myelin. Here, we show that TRPA1 is constitutively active in oligodendrocytes and the optic nerve, as the specific TRPA1 antagonist, A-967079, decreases basal oligodendrocyte Ca2+ concentrations and increases the size of the compound action potential (CAP). Conversely, TRPA1 agonists reduce the size of the optic nerve CAP in an A-967079-sensitive manner. These results indicate that glial TRPA1 regulates neuronal excitability in the white matter under physiological as well as pathological conditions. Importantly, we find that inhibition of TRPA1 prevents loss of CAPs during oxygen and glucose deprivation (OGD) and improves the recovery. TRPA1 block was effective when applied before, during, or after OGD, indicating that the TRPA1-mediated damage is occurring during both ischaemia and recovery, but importantly, that therapeutic intervention is possible after the ischaemic insult. These results indicate that TRPA1 has an important role in the brain, and that its block may be effective in treating many white matter diseases. Full article
(This article belongs to the Special Issue TRPA1 Receptor as a Potential Therapeutic Target in Pain, Inflammation and Neurodegeneration)
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17 pages, 1688 KiB  
Article
Periorbital Nociception in a Progressive Multiple Sclerosis Mouse Model Is Dependent on TRPA1 Channel Activation
by Diéssica Padilha Dalenogare, Camila Ritter, Fernando Roberto Antunes Bellinaso, Sabrina Qader Kudsi, Gabriele Cheiran Pereira, Maria Fernanda Pessano Fialho, Débora Denardin Lückemeyer, Caren Tatiane de David Antoniazzi, Lorenzo Landini, Juliano Ferreira, Guilherme Vargas Bochi, Sara Marchesan Oliveira, Francesco De Logu, Romina Nassini, Pierangelo Geppetti and Gabriela Trevisan
Pharmaceuticals 2021, 14(8), 831; https://doi.org/10.3390/ph14080831 - 23 Aug 2021
Cited by 10 | Viewed by 3358
Abstract
Headaches are frequently described in progressive multiple sclerosis (PMS) patients, but their mechanism remains unknown. Transient receptor potential ankyrin 1 (TRPA1) was involved in neuropathic nociception in a model of PMS induced by experimental autoimmune encephalomyelitis (PMS-EAE), and TRPA1 activation causes periorbital and [...] Read more.
Headaches are frequently described in progressive multiple sclerosis (PMS) patients, but their mechanism remains unknown. Transient receptor potential ankyrin 1 (TRPA1) was involved in neuropathic nociception in a model of PMS induced by experimental autoimmune encephalomyelitis (PMS-EAE), and TRPA1 activation causes periorbital and facial nociception. Thus, our purpose was to observe the development of periorbital mechanical allodynia (PMA) in a PMS-EAE model and evaluate the role of TRPA1 in periorbital nociception. Female PMS-EAE mice elicited PMA from day 7 to 14 days after induction. The antimigraine agents olcegepant and sumatriptan were able to reduce PMA. The PMA was diminished by the TRPA1 antagonists HC-030031, A-967079, metamizole and propyphenazone and was absent in TRPA1-deficient mice. Enhanced levels of TRPA1 endogenous agonists and NADPH oxidase activity were detected in the trigeminal ganglion of PMS-EAE mice. The administration of the anti-oxidants apocynin (an NADPH oxidase inhibitor) or alpha-lipoic acid (a sequestrant of reactive oxygen species), resulted in PMA reduction. These results suggest that generation of TRPA1 endogenous agonists in the PMS-EAE mouse model may sensitise TRPA1 in trigeminal nociceptors to elicit PMA. Thus, this ion channel could be a potential therapeutic target for the treatment of headache in PMS patients. Full article
(This article belongs to the Special Issue TRPA1 Receptor as a Potential Therapeutic Target in Pain, Inflammation and Neurodegeneration)
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