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Molecular and Cellular Mechanisms of Spinal Cord Injury and Repair

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: 25 April 2025 | Viewed by 1678

Special Issue Editor


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Guest Editor
Neuronal and Tissue Regeneration Laboratory, Centro de Investigación Príncipe Felipe (CIPF), Valencia, Spain
Interests: spinal cord injury repair; cell and gene therapy; biomaterials; neural stimulation

Special Issue Information

Dear Colleagues,

Spinal cord injury (SCI) is a devastating, debilitating, and life-altering condition that currently lacks a cure or effective treatment. After SCI, the descending and ascending communication from the brain to the peripheral sensors and vice versa are abruptly altered. Because of the primary trauma and the consequent secondary damage and loss of innervation, a cascade of degenerating and adaptive responses is activated. The main goal of this Special Issue is to focus on collecting new advances describing the molecular and cellular mechanisms involved in the SCI pathological process, as well as adaptative spontaneous responses and therapeutical approaches. Novel transcriptional regulations, funtional neuronal, glial, or other infiltrated cell entity responses, or therapeutical molecular or cellular experimental approaches will highly contribute to better defining the molecular and cellular scenario of the injured spinal cord and the consequent structural and funtional adaptive process.

Dr. Victoria Moreno-Manzano
Guest Editor

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Keywords

  • spinal cord injury
  • molecular changes
  • neuronal degeneration
  • circuit regeneration
  • transcriptomics
  • cell imaging
  • single-cell analysis
  • cell communication
  • behavior
  • functional outputs

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Published Papers (2 papers)

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Research

14 pages, 5933 KiB  
Article
Long-Term 5-HT1A Receptor Agonist NLX-112 Treatment Improves Functional Recovery After Spinal Cord Injury
by Ching-Yi Lin, Kevin Li, Thomas Gitchell and Yu-Shang Lee
Int. J. Mol. Sci. 2025, 26(1), 239; https://doi.org/10.3390/ijms26010239 - 30 Dec 2024
Viewed by 461
Abstract
Spinal cord injury (SCI) results in functional deficits below the injured spinal level. The descending serotonergic system in the spinal cord is critically involved in the control of motor and autonomic functions. Specifically, SCI damages the projections of serotonergic fibers, which leads to [...] Read more.
Spinal cord injury (SCI) results in functional deficits below the injured spinal level. The descending serotonergic system in the spinal cord is critically involved in the control of motor and autonomic functions. Specifically, SCI damages the projections of serotonergic fibers, which leads to reduced serotonin inputs and increased amounts of spinal serotonergic receptors. Our previous pharmacological study demonstrated that brief administration of a highly selective 5-HT1A receptor agonist, NLX-112, improves lower urinary tract (LUT) function at the termination stage of thoracic 8 (T8) contusive SCI in rats. However, whether chronic activation of serotonin 5-HT1A receptors by NLX-112 after SCI is beneficial remains an unanswered question. Here, we evaluated the efficacy of long-term NLX-112 intervention starting from two weeks post-T8 contusive SCI for an additional six weeks. We evaluated locomotion, LUT function, bladder morphology, and the number of spinal 5-HT1A receptors in both L4 and L6/S1 spinal cord segments. Our results indicate that NLX-112 treatment significantly improves locomotion in a dose-dependent fashion, improves LUT function, reduces bladder weight and bladder wall thickness, and reduces the SCI-upregulated spinal 5-HT1A receptors compared to vehicle-treated SCI animals. These data suggest promising therapeutic potential for long-term NLX-112 activation of 5-HT1A receptors to treat SCI. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Spinal Cord Injury and Repair)
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14 pages, 5581 KiB  
Article
Noggin-Loaded PLA/PCL Patch Inhibits BMP-Initiated Reactive Astrogliosis
by James Hawes, Ana Gonzalez-Manteiga, Kendall P. Murphy, Marina Sanchez-Petidier, Victoria Moreno-Manzano, Bedika Pathak, Kristin Lampe, Chia-Ying Lin, Jose L. Peiro and Marc Oria
Int. J. Mol. Sci. 2024, 25(21), 11626; https://doi.org/10.3390/ijms252111626 - 29 Oct 2024
Cited by 1 | Viewed by 864
Abstract
Myelomeningocele (MMC) is a congenital birth defect of the spine and spinal cord, commonly treated clinically through prenatal or postnatal surgery by repairing the unclosed spinal canal. Having previously developed a PLA/PCL polymer smart patch for this condition, we aim to further expand [...] Read more.
Myelomeningocele (MMC) is a congenital birth defect of the spine and spinal cord, commonly treated clinically through prenatal or postnatal surgery by repairing the unclosed spinal canal. Having previously developed a PLA/PCL polymer smart patch for this condition, we aim to further expand the potential therapeutic options by providing additional cellular and biochemical support in addition to its mechanical properties. Bone morphogenetic proteins (BMPs) are a large class of secreted factors that serve as modulators of development in multiple organ systems, including the CNS. We hypothesize that our smart patch mitigates the astrogenesis induced, at least partly, by increased BMP activity during MMC. To test this hypothesis, neural stem or precursor cells were isolated from rat fetuses and cultured in the presence of Noggin, an endogenous antagonist of BMP action, with recombinant BMPs. We found that the developed PLA/PCL patch not only serves as a biocompatible material for developing neural stem cells but was also able to act as a carrier for BMP–Notch pathway inhibitor Noggin, effectively minimizing the effect of BMP2 or BMP4 on NPCs cultured with the Noggin-loaded patch. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Spinal Cord Injury and Repair)
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