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New Insights into the Molecular Mechanisms of Chronic Pain
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New Insights into the Molecular Mechanisms of Chronic Pain

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: 20 October 2024 | Viewed by 677

Special Issue Editors

Dr. Fani L. Neto

E-Mail Website
Guest Editor
Departamento de Biomedicina–Unidade de Biologia Experimental, Faculdade de Medicina, Universidade do Porto, Alameda Prof. Hernâni Monteiro, 4200-319 Porto, Portugal
Interests: glial cells; dorsal root ganglia; descending pain modulation
Dr. Isabel Martins

E-Mail Website
Guest Editor
Departamento de Biomedicina–Unidade de Biologia Experimental, Faculdade de Medicina, Universidade do Porto, Alameda Prof. Hernâni Monteiro, 4200-319 Porto, Portugal
Interests: descending pain modulation; opioids; diffuse noxious inhibitory controls (DNIC)

Special Issue Information

Dear Colleagues,

Chronic pain of various aetiologies affects a high percentage of the population worldwide and is responsible for high costs to society. It is associated with several comorbidities that negatively impact the quality of life of patients and their close relatives. Chronic pain is considered a disease on its own, but the available treatments are not always effective and present many side effects. Despite the progress made in the last few decades towards understanding chronic pain neurobiology, there is still a large gap regarding the role of many cell types, molecules and their receptors, and the molecular identity of all the pathways involved. In particular, the molecular characterization of the circuitries implicated in descending modulation as well as those related with the cognitive and affective dimensions of pain is still underexplored. Also relevant, but poorly investigated, are the differences between sexes in pain circuitries and how they affect chronic pain. In this Special Issue, we welcome all manuscripts bringing new insights into these topics.

Dr. Fani L. Neto
Dr. Isabel Martins
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

  • dorsal root ganglia
  • spinal cord
  • brain
  • opioids
  • monoamines
  • GABA
  • anxiety
  • depression
  • cognition
  • optogenetics
  • electrophysiology
  • behavior
  • glial cells

Published Papers (1 paper)

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Research

18 pages, 7236 KiB  
Article
MIF-Modulated Spinal Proteins Associated with Persistent Bladder Pain: A Proteomics Study
by Shaojing Ye, Nilesh M. Agalave, Fei Ma, Dlovan F. D. Mahmood, Asma Al-Grety, Payam E. Khoonsari, Lin Leng, Camilla I. Svensson, Richard Bucala, Kim Kultima and Pedro L. Vera
Int. J. Mol. Sci. 2024, 25(8), 4484; https://doi.org/10.3390/ijms25084484 - 19 Apr 2024
Viewed by 348
Abstract
Bladder pain is a prominent symptom in Interstitial Cystitis/Bladder Pain Syndrome (IC/BPS). We studied spinal mechanisms of bladder pain in mice using a model where repeated activation of intravesical Protease Activated Receptor-4 (PAR4) results in persistent bladder hyperalgesia (BHA) with little or no [...] Read more.
Bladder pain is a prominent symptom in Interstitial Cystitis/Bladder Pain Syndrome (IC/BPS). We studied spinal mechanisms of bladder pain in mice using a model where repeated activation of intravesical Protease Activated Receptor-4 (PAR4) results in persistent bladder hyperalgesia (BHA) with little or no bladder inflammation. Persistent BHA is mediated by spinal macrophage migration inhibitory factor (MIF), and is associated with changes in lumbosacral proteomics. We investigated the contribution of individual spinal MIF receptors to persistent bladder pain as well as the spinal proteomics changes associated with relief of persistent BHA by spinal MIF antagonism. Female mice with persistent BHA received either intrathecal (i.t.) MIF monoclonal antibodies (mAb) or mouse IgG1 (isotype control antibody). MIF antagonism temporarily reversed persistent BHA (peak effect: 2 h), while control IgG1 had no effect. Moreover, i.t. antagonism of the MIF receptors CD74 and C-X-C chemokine receptor type 4 (CXCR4) partially reversed persistent BHA. For proteomics experiments, four separate groups of mice received either repeated intravesical scrambled peptide and sham i.t. injection (control, no pain group) or repeated intravesical PAR4 and: sham i.t.; isotype IgG1 i.t. (15 μg); or MIF mAb (15 μg). L6-S1 spinal segments were excised 2 h post-injection and examined for proteomics changes using LC-MS/MS. Unbiased proteomics analysis identified and relatively quantified 6739 proteins. We selected proteins that showed significant changes compared to control (no pain group) after intravesical PAR4 (sham or IgG i.t. treatment) and showed no significant change after i.t. MIF antagonism. Six proteins decreased during persistent BHA (V-set transmembrane domain-containing protein 2-like confirmed by immunohistochemistry), while two proteins increased. Spinal MIF antagonism reversed protein changes. Therefore, spinal MIF and MIF receptors mediate persistent BHA and changes in specific spinal proteins. These novel MIF-modulated spinal proteins represent possible new targets to disrupt spinal mechanisms that mediate persistent bladder pain. Full article
(This article belongs to the Special Issue New Insights into the Molecular Mechanisms of Chronic Pain)
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