ijms-logo

Journal Browser

Journal Browser

Molecular Mechanisms of Pain 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 May 2022)

Special Issue Editors


E-Mail Website
Guest Editor
Department of Medicine, Surgery and Neuroscience, University of Siena, 53100 Siena, Italy
Interests: chronic pain; pain measurement; pain biology
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Institute of Physiology, University of Siena, Siena, Italy
Interests: nociception QST pain in newborns and infants; pain congenital insensitivity and hyposensitivity

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our 2020 Special Issue “Molecular Mechanisms of Pain”.

Painful thermal, mechanical and chemical stimuli can reach the nervous system and change it. Short- as well as long-lasting pain activate both the peripheral and central nervous system components of pain transmission pathways. All these components exhibit plasticity, i.e., changes that persist. The short-term consequences of this are hyperalgesia and allodynia, while chronic pain is a long-term consequence. A huge number of molecular mechanisms, sometimes immune activity-dependent, have been described to explain these changes; many of these are different between male and female subjects. New genes, old hormones, and novel drugs have recently been added to the pain modulation picture. In this Special Issue, new and old schemas will be presented to update a serious health problem.

Prof. Dr. Anna Maria Aloisi
Dr. Valeria Bachiocco
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • nociceptors
  • pain pathways
  • plasticity
  • sex differences
  • gonadal hormones
  • immune-mediated mechanisms
  • receptors
  • gene expression
  • enzymes
  • development
  • drugs

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

14 pages, 2649 KiB  
Article
Nogo-A Induced Polymerization of Microtubule Is Involved in the Inflammatory Heat Hyperalgesia in Rat Dorsal Root Ganglion Neurons
by Ling Chen, Qiguo Hu, Huaicun Liu, Yan Zhao, Sun-On Chan and Jun Wang
Int. J. Mol. Sci. 2021, 22(19), 10360; https://doi.org/10.3390/ijms221910360 - 26 Sep 2021
Viewed by 2146
Abstract
The microtubule, a major constituent of cytoskeletons, was shown to bind and interact with transient receptor potential vanilloid subfamily member 1 (TRPV1), and serves a pivotal role to produce thermal hyperalgesia in inflammatory pain. Nogo-A is a modulator of microtubule assembly and plays [...] Read more.
The microtubule, a major constituent of cytoskeletons, was shown to bind and interact with transient receptor potential vanilloid subfamily member 1 (TRPV1), and serves a pivotal role to produce thermal hyperalgesia in inflammatory pain. Nogo-A is a modulator of microtubule assembly and plays a key role in maintaining the function of TRPV1 in inflammatory heat pain. However, whether the microtubule dynamics modulated by Nogo-A in dorsal root ganglion (DRG) neurons participate in the inflammatory pain is not elucidated. Here we reported that the polymerization of microtubules in the DRG neurons, as indicated by the acetylated α-tubulin, tubulin polymerization-promoting protein 3 (TPPP3), and microtubule numbers, was significantly elevated in the complete Freund’s adjuvant (CFA) induced inflammatory pain. Consistent with our previous results, knock-out (KO) of Nogo-A protein significantly attenuated the heat hyperalgesia 72 h after CFA injection and decreased the microtubule polymerization via up-regulation of phosphorylation of collapsin response mediator protein 2 (CRMP2) in DRG. The colocalization of acetylated α-tubulin and TRPV1 in DRG neurons was also reduced dramatically in Nogo-A KO rats under inflammatory pain. Moreover, the down-regulation of TRPV1 in DRG of Nogo-A KO rats after injection of CFA was reversed by intrathecal injection of paclitaxel, a microtubule stabilizer. Furthermore, intrathecal injection of nocodazole (a microtubule disruptor) attenuated significantly the CFA-induced inflammatory heat hyperalgesia and the mechanical pain in a rat model of spared nerve injury (SNI). In these SNI cases, the Nogo-A and acetylated α-tubulin in DRG were also significantly up-regulated. We conclude that the polymerization of microtubules promoted by Nogo-A in DRG contributes to the development of inflammatory heat hyperalgesia mediated by TRPV1. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Pain 2.0)
Show Figures

Figure 1

Review

Jump to: Research

29 pages, 2061 KiB  
Review
DNA Methylation and Non-Coding RNAs during Tissue-Injury Associated Pain
by Jahanzaib Irfan, Muhammad Rizki Febrianto, Anju Sharma, Thomas Rose, Yasamin Mahmudzade, Simone Di Giovanni, Istvan Nagy and Jose Vicente Torres-Perez
Int. J. Mol. Sci. 2022, 23(2), 752; https://doi.org/10.3390/ijms23020752 - 11 Jan 2022
Cited by 6 | Viewed by 4072
Abstract
While about half of the population experience persistent pain associated with tissue damages during their lifetime, current symptom-based approaches often fail to reduce such pain to a satisfactory level. To provide better patient care, mechanism-based analgesic approaches must be developed, which necessitates a [...] Read more.
While about half of the population experience persistent pain associated with tissue damages during their lifetime, current symptom-based approaches often fail to reduce such pain to a satisfactory level. To provide better patient care, mechanism-based analgesic approaches must be developed, which necessitates a comprehensive understanding of the nociceptive mechanism leading to tissue injury-associated persistent pain. Epigenetic events leading the altered transcription in the nervous system are pivotal in the maintenance of pain in tissue injury. However, the mechanisms through which those events contribute to the persistence of pain are not fully understood. This review provides a summary and critical evaluation of two epigenetic mechanisms, DNA methylation and non-coding RNA expression, on transcriptional modulation in nociceptive pathways during the development of tissue injury-associated pain. We assess the pre-clinical data and their translational implication and evaluate the potential of controlling DNA methylation and non-coding RNA expression as novel analgesic approaches and/or biomarkers of persistent pain. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Pain 2.0)
Show Figures

Figure 1

Back to TopTop