Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.1
4.9
Journals
IJMS
Special Issues
Editorial Board Members’ Collection Series: “Neuroinflammation”
ijms-logo
Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Editorial Board Members’ Collection Series: “Neuroinflammation”

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 20 October 2024 | Viewed by 1577

Special Issue Editors

Dr. Savina Apolloni

E-Mail Website
Guest Editor
Department of Biology, Tor Vergata University of Rome, 00133 Rome, Italy
Interests: molecular mechanisms of neurodegeneration; amyotrophic lateral sclerosis; neuroinflammation; microglia; fibrosis; astrocytes; animal models of neurodegenerative diseases; purinergic signaling; histaminergic signaling; neuropharmacology
Special Issues, Collections and Topics in MDPI journals
Dr. Sushruta Koppula

E-Mail Website
Guest Editor
Department of Biotechnology, Konkuk University, Chungju 380, Republic of Korea
Interests: neurodegeneration

Special Issue Information

Dear Colleagues,

The Editorial Board Members’ Collection Series: “Neuroinflammation” aims to collect high-quality research articles, short communications, and review articles in all fields of neuroinflammation. We encourage Editorial Board Members of the Molecular Immunology, Neurobiology, and Pharmacology Sections of the International Journal of Molecular Sciences to contribute papers reflecting the latest progress in their research field.

Topics include, but are not limited to, the following:
  • Neuroinflammation in Amyotrophic Lateral Sclerosis;
  • Neuroinflammation in Multiple Sclerosis;
  • Neuroinflammation in Parkinson's disease;
  • Neuroinflammation in Alzheimer's disease;
  • Neuroinflammation in Ataxias;
  • Neuroinflammation in Traumatic Brain Injury;
  • Neuroinflammation in Spinal Cord Injury;
  • Drugs targeting Neuroinflammation.

Dr. Savina Apolloni
Dr. Sushruta Koppula
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

  • neuroinflammation
  • amyotrophic lateral sclerosis
  • multiple sclerosis
  • Parkinson's disease
  • Alzheimer's disease
  • ataxias
  • traumatic brain injury
  • spinal cord injury

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

13 pages, 2091 KiB  
Article
Anti-Neuroinflammatory Effects of a Novel Bile Acid Derivative
by Srđan Bjedov, Goran Stegnjaić, Suzana Stanisavljević, Milica Lazarević, Ivan Pilipović, Marija Sakač and Đorđe Miljković
Int. J. Mol. Sci. 2024, 25(13), 7136; https://doi.org/10.3390/ijms25137136 - 28 Jun 2024
Viewed by 214
Abstract
In the search for novel potent immunomodulatory nuclear factor-erythroid 2 related factor 2 (Nrf2) activators, a derivative of cholic bile acid, SB140, was synthesized. The synthesis of SB140 aimed to increase the electrophilic functionality of the compound, enhancing its ability to activate Nrf2. [...] Read more.
In the search for novel potent immunomodulatory nuclear factor-erythroid 2 related factor 2 (Nrf2) activators, a derivative of cholic bile acid, SB140, was synthesized. The synthesis of SB140 aimed to increase the electrophilic functionality of the compound, enhancing its ability to activate Nrf2. Effects of SB140 on microglial cells, myeloid-derived cells (MDC), and T cells were explored in the context of (central nervous system) CNS autoimmunity. SB140 potently activated Nrf2 signaling in MDC and microglia. It was efficient in reducing the ability of microglial cells to produce inflammatory nitric oxide, interleukin (IL)-6, and tumor necrosis factor (TNF). Also, SB140 reduced the proliferation of encephalitogenic T cells and the production of their effector cytokines: IL-17 and interferon (IFN)-γ. On the contrary, the effects of SB140 on anti-inflammatory IL-10 production in microglial and encephalitogenic T cells were limited or absent. These results show that SB140 is a potent Nrf2 activator, as well as an immunomodulatory compound. Thus, further research on the application of SB140 in the treatment of neuroinflammatory diseases is warranted. Animal models of multiple sclerosis and other inflammatory neurological disorders will be a suitable choice for such studies. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: “Neuroinflammation”)
►▼ Show Figures

Graphical abstract

16 pages, 3991 KiB  
Article
Human C15orf39 Inhibits Inflammatory Response via PRMT2 in Human Microglial HMC3 Cell Line
by Min Zhang, Yaqi Xu, Gaizhi Zhu, Qi Zeng, Ran Gao, Jinming Qiu, Wenting Su and Renxi Wang
Int. J. Mol. Sci. 2024, 25(11), 6025; https://doi.org/10.3390/ijms25116025 - 30 May 2024
Viewed by 371
Abstract
Microglia-mediated inflammatory response is one key cause of many central nervous system diseases, like Alzheimer’s disease. We hypothesized that a novel C15orf39 (MAPK1 substrate) plays a critical role in the microglial inflammatory response. To confirm this hypothesis, we used lipopolysaccharide (LPS)-and interferon-gamma (IFN-γ)-induced [...] Read more.
Microglia-mediated inflammatory response is one key cause of many central nervous system diseases, like Alzheimer’s disease. We hypothesized that a novel C15orf39 (MAPK1 substrate) plays a critical role in the microglial inflammatory response. To confirm this hypothesis, we used lipopolysaccharide (LPS)-and interferon-gamma (IFN-γ)-induced human microglia HMC3 cells as a representative indicator of the microglial in vitro inflammatory response. We found that C15orf39 was down-regulated when interleukin-6 (IL-6) and tumor necrosis factor-α (TNFα) expression increased in LPS/IFN-γ-stimulated HMC3 cells. Once C15orf39 was overexpressed, IL-6 and TNFα expression were reduced in LPS/IFN-γ-stimulated HMC3 cells. In contrast, C15orf39 knockdown promoted IL-6 and TNFα expression in LPS/IFN-γ-stimulated HMC3 cells. These results suggest that C15orf39 is a suppressive factor in the microglial inflammatory response. Mechanistically, C15orf39 interacts with the cytoplasmic protein arginine methyltransferase 2 (PRMT2). Thus, we termed C15orf39 a PRMT2 interaction protein (PRMT2 IP). Furthermore, the interaction of C15orf39 and PRMT2 suppressed the activation of NF-κB signaling via the PRMT2-IκBα signaling axis, which then led to a reduction in transcription of the inflammatory factors IL6 and TNF-α. Under inflammatory conditions, NF-κBp65 was found to be activated and to suppress C15orf39 promoter activation, after which it canceled the suppressive effect of the C15orf39-PRMT2-IκBα signaling axis on IL-6 and TNFα transcriptional expression. In conclusion, our findings demonstrate that in a steady condition, the interaction of C15orf39 and PRMT2 stabilizes IκBα to inhibit IL-6 and TNFα expression by suppressing NF-κB signaling, which reversely suppresses C15orf39 transcription to enhance IL-6 and TNFα expression in the microglial inflammatory condition. Our study provides a clue as to the role of C15orf39 in microglia-mediated inflammation, suggesting the potential therapeutic efficacy of C15orf39 in some central nervous system diseases. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: “Neuroinflammation”)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop