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Special Issue "Neuroprotective Strategies 2019"

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

Deadline for manuscript submissions: 31 December 2019

Special Issue Editor

Guest Editor
Prof. Dr. Katalin Prokai-Tatrai

Department of Pharmacology and Neuroscience, University of North Texas Health Science Center, 3500 Camp Bowie Blvd, Fort Worth, TX 76107, USA
Website | E-Mail
Interests: drug design of central nervous system agents; neuropeptides and peptidomimetics; prodrugs for CNS delivery; CNS-selective estrogen therapy; neuroprotection; proteomics

Special Issue Information

Dear Colleagues,

It has been 10 years since we started the “Neuroprotective Strategies” collection, offering the latest information on neuroprotection through the preclinical/basic science assessments of the various in vitro and animal models relevant to neurodegeneration, drug discovery efforts, and clinical case reports. We hope that this Special Issue will continue to provide a forum for thought-provoking comments, opinions, and perspectives, in addition to traditional reviews and research articles on the latest developments of therapeutics in the field. We especially encourage submissions that address the critical issues that have prevented successful the clinical translations of otherwise promising laboratory data. These issues include the limitations of in vitro studies and preclinical animal models to mirror the multiple pathologies underlying human neurodegenerative diseases, the lack of drug-likeness of experimental agents, obstacles of drug delivery to the CNS, and the consideration of ADMET and pharmacokinetics, especially in early stage drug discovery. Critical reviews of relevant patent literature and clinical findings are also welcome. I wish to thank all of the authors for their exceptional contributions to this Special Issue over the years, and I look forward to receiving future contributions to the 10th anniversary issue on the promising and challenging aspects of neuroprotective strategies. I hope this topical collection has been, and will continue to be, a useful reference for everybody interested in the subject.

Prof. Dr. Katalin Prokai-Tatrai
Guest Editor

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 papers will be 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. The Article Processing Charge (APC) for publication in this open access journal is 1800 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

  • Clinical case report
  • CNS-targeting drug design and drug-likeness
  • Inflammation
  • Drug delivery
  • In-silico drug design and disease models
  • Ischemia and reperfusion
  • Ocular neurodegeneration
  • Oxidative stress
  • Peripheral nervous system
  • Proteomics
  • Spinal cord injury
  • Stroke
  • Structure–activity relationships
  • Translational medicine
  • Traumatic brain injury

Related Special Issue

Published Papers (2 papers)

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Research

Open AccessArticle
RTA 408 Inhibits Interleukin-1β-Induced MMP-9 Expression via Suppressing Protein Kinase-Dependent NF-κB and AP-1 Activation in Rat Brain Astrocytes
Int. J. Mol. Sci. 2019, 20(11), 2826; https://doi.org/10.3390/ijms20112826
Received: 20 May 2019 / Revised: 3 June 2019 / Accepted: 7 June 2019 / Published: 10 June 2019
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Abstract
Neuroinflammation is characterized by the elevated expression of various inflammatory proteins, including matrix metalloproteinases (MMPs), induced by various pro-inflammatory mediators, which play a critical role in neurodegenerative disorders. Interleukin-1β (IL-1β) has been shown to induce the upregulation of MMP-9 through nicotinamide adenine dinucleotide [...] Read more.
Neuroinflammation is characterized by the elevated expression of various inflammatory proteins, including matrix metalloproteinases (MMPs), induced by various pro-inflammatory mediators, which play a critical role in neurodegenerative disorders. Interleukin-1β (IL-1β) has been shown to induce the upregulation of MMP-9 through nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX)-reactive oxygen species (ROS)-dependent signaling pathways. N-(2-cyano-3,12-dioxo-28-noroleana-1,9(11)-dien-17-yl)-2-2-difluoropropanamide (RTA 408), a novel synthetic triterpenoid, has been shown to possess anti-oxidant and anti-inflammatory properties in various types of cells. Here, we evaluated the effects of RTA 408 on IL-1β-induced inflammatory responses by suppressing MMP-9 expression in a rat brain astrocyte (RBA-1) line. IL-1β-induced MMP-9 protein and mRNA expression, and promoter activity were attenuated by RTA 408. The increased level of ROS generation in RBA-1 cells exposed to IL-1β was attenuated by RTA 408, as determined by using 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) and CellROX. In addition, the inhibitory effects of RTA 408 on MMP-9 expression resulted from the suppression of the IL-1β-stimulated activation of Pyk2 (proline-rich tyrosine kinase), platelet-derived growth factor receptor β (PDGFRβ), Akt, ROS, and mitogen-activated protein kinases (MAPKs). Pretreatment with RTA 408 attenuated the IL-1β-induced c-Jun phosphorylation, mRNA expression, and promoter activity. IL-1β-stimulated nuclear factor-κB (NF-κB) p65 phosphorylation, translocation, and promoter activity were also attenuated by RTA 408. Furthermore, IL-1β-induced glial fibrillary acidic protein (GFAP) protein and mRNA expression, and cell migration were attenuated by pretreatment with RTA 408. These results provide new insights into the mechanisms by which RTA 408 attenuates IL-1β-mediated inflammatory responses and exerts beneficial effects for the management of brain diseases. Full article
(This article belongs to the Special Issue Neuroprotective Strategies 2019)
Figures

Graphical abstract

Open AccessArticle
Niemann-Pick Type A Disease: Behavior of Neutral Sphingomyelinase and Vitamin D Receptor
Int. J. Mol. Sci. 2019, 20(9), 2365; https://doi.org/10.3390/ijms20092365
Received: 22 March 2019 / Revised: 3 May 2019 / Accepted: 7 May 2019 / Published: 13 May 2019
PDF Full-text (2090 KB) | HTML Full-text | XML Full-text
Abstract
Sphingomyelinase (SMase) is responsible for the breakdown of sphingomyelin (SM) with production of ceramide. The absence of acid sphingomyelinase (aSMase) causes abnormal synapse formation in Niemann-Pick type A (NPA) disease. Because high levels of ceramide in the NPA brain were demonstrated, the involvement [...] Read more.
Sphingomyelinase (SMase) is responsible for the breakdown of sphingomyelin (SM) with production of ceramide. The absence of acid sphingomyelinase (aSMase) causes abnormal synapse formation in Niemann-Pick type A (NPA) disease. Because high levels of ceramide in the NPA brain were demonstrated, the involvement of other SMases were supposed. In the present study we focused the attention on the neurogenic niches in the hippocampal gyrus dentatus (GD), a brain structure essential for forming cohesive memory. We demonstrated for the first time the increase of (Sex determining region Y)-box 2 (SOX2), and the down-regulation of glial fibrillary acidic protein (GFAP) NPA mice GD. Moreover, we found that the expression of Toll like receptors (TLRs), was increased in NPA mice, particularly TLR2, TLR7, TLR8 and TLR9 members. Although no significant change in neutral sphingomyelinase (nSMase) gene expression was detected in the NPA mice hippocampus of, protein levels were enhanced, probably because of the slower protein degradation rate in this area. Many studies demonstrated that vitamin D receptor (VDR) is expressed in the hippocampus GD. Unexpectedly, we showed that NPA mice exhibited VDR gene and protein expression up-regulation. In summary, our study suggests a relation between hippocampal cell differentiation defect, nSMase and VDR increase in NPA mice. Full article
(This article belongs to the Special Issue Neuroprotective Strategies 2019)
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Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
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