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Molecular Research in Spinal Cord Injury
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Molecular Research in Spinal Cord Injury

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: 20 May 2025 | Viewed by 5254

Special Issue Editor

Prof. Dr. Inbo Han

E-Mail Website
Guest Editor
Department of Neurosurgery, CHA University School of Medicine, CHA Bundang Medical Center, Seongnam-si 13496, Republic of Korea
Interests: spinal diseases (spinal cord injury, intervertebral disc degeneration, osteoporosis, etc.); pain; regeneration; stem cell; neuroprotection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to announce a Special Issue on “Molecular Research in Spinal Cord Injury” in the International Journal of Molecular Sciences (IJMS). This Special Issue aims to highlight cutting-edge research and advancements in the molecular mechanisms underlying spinal cord injuries (SCIs).

The scope of this Special Issue will cover a wide range of topics, including but not limited to, the following:

  • Molecular and cellular responses to spinal cord injury;
  • Stem cell therapy and regenerative medicine;
  • Tissue engineering approaches for spinal cord repair;
  • Neuroinflammation and neuroprotection;
  • Genetic and epigenetic regulation in SCIs;
  • Innovative therapeutic strategies.

This Special Issue seeks to gather contributions from leading researchers and practitioners in the field. By sharing new insights and developments, we hope to foster a deeper understanding and facilitate advancements in the treatment and management of spinal cord injuries.

Prof. Dr. Inbo Han
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 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

  • spinal cord injury
  • molecular mechanisms
  • stem cell therapy
  • tissue engineering
  • neuroinflammation
  • neuroprotection
  • genetic regulation
  • epigenetics
  • therapeutic strategies

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Published Papers (3 papers)

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Research

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19 pages, 4085 KiB  
Article
Transcriptomic Profiling of Primary Microglia: Effects of miR-19a-3p and miR-19b-3p on Microglia Activation
by Faezeh Sahebdel, Aliabbas Zia, Hector Ramiro Quinta, Leslie R. Morse, Julie K. Olson and Ricardo A. Battaglino
Int. J. Mol. Sci. 2024, 25(19), 10601; https://doi.org/10.3390/ijms251910601 - 1 Oct 2024
Viewed by 1216
Abstract
Neuropathic pain resulting from spinal cord injury (SCI) is a significant secondary health issue affecting around 60% of individuals with SCI. After SCI, activation of microglia, the immune cells within the central nervous system, leads to neuroinflammation by producing pro-inflammatory cytokines and affects [...] Read more.
Neuropathic pain resulting from spinal cord injury (SCI) is a significant secondary health issue affecting around 60% of individuals with SCI. After SCI, activation of microglia, the immune cells within the central nervous system, leads to neuroinflammation by producing pro-inflammatory cytokines and affects neuropathic pain. This interplay between inflammation and pain contributes to the persistent and intense pain experienced by many individuals with SCI. MicroRNAs (miRs) have been critical regulators of neuroinflammation. Previous research in our laboratory has revealed upregulation levels of circulating miR-19a and miR-19b in individuals with SCI with neuropathic pain compared to those without pain. In this study, we treated primary microglial cultures from mice with miR-19a and miR-19b for 24 h and conducted RNA sequencing analysis. Our results showed that miR-19a and miR-19b up- and downregulate different genes according to the volcano plots and the heatmaps. miR-19a and miR-19b regulate inflammation through distinct signaling pathways. The results showed that miR-19a promotes inflammation via toll-like receptor signaling, TNF signaling, and cytokine–cytokine receptor interactions, while miR-19b increases inflammatory responses through the PI3K-Akt signaling pathway, focal adhesion, and extracellular matrix receptor interactions. The protein–protein interaction (PPI) networks used the STRING database to identify transcription factors associated with genes up- or downregulated by miR-19a and miR-19b. Key transcription factors, such as STAT1, STAT2, and KLF4 for miR-19a, and Nr4a1, Nr4a2, and Nr4a3 for miR-19b, were identified and revealed their roles in regulating neuroinflammation. This study demonstrates that miR-19a and miR-19b modulate diverse patterns of gene expression, regulate inflammation, and induce inflammatory responses in microglia. Full article
(This article belongs to the Special Issue Molecular Research in Spinal Cord Injury)
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16 pages, 2744 KiB  
Article
Regeneration and Plasticity Induced by Epidural Stimulation  in a Rodent Model of Spinal Cord Injury
by Leonidas Gomes Angelin, Marcelo Nelson Páez Carreño, Jose Pinhata Otoch, Joyce Cristina Ferreira de Resende, Analía Arévalo, Lívia Clemente Motta-Teixeira, Marilia Cerqueira Leite Seelaender and Guilherme Lepski
Int. J. Mol. Sci. 2024, 25(16), 9043; https://doi.org/10.3390/ijms25169043 - 21 Aug 2024
Cited by 2 | Viewed by 2071
Abstract
Traumatic spinal cord injury is a major cause of disability for which there are currently no fully effective treatments. Recent studies using epidural electrical stimulation have shown significant advances in motor rehabilitation, even when applied during chronic phases of the disease. The present [...] Read more.
Traumatic spinal cord injury is a major cause of disability for which there are currently no fully effective treatments. Recent studies using epidural electrical stimulation have shown significant advances in motor rehabilitation, even when applied during chronic phases of the disease. The present study aimed to investigate the effectiveness of epidural electric stimulation in the motor recovery of rats with spinal cord injury. Furthermore, we aimed to elucidate the neurophysiological mechanisms underlying motor recovery. First, we improved upon the impact spinal cord injury model to cause severe and permanent motor deficits lasting up to 2 months. Next, we developed and tested an implantable epidural spinal cord stimulator device for rats containing an electrode and an implantable generator. Finally, we evaluated the efficacy of epidural electrical stimulation on motor recovery after spinal cord injury in Wistar rats. A total of 60 animals were divided into the following groups: (i) severe injury with epidural electrical stimulation (injury + stim, n = 15), (ii) severe injury without stimulation (group injury, n = 15), (iii) sham implantation without battery (sham, n = 15), and (iv) a control group, without surgical intervention (control, n = 15). All animals underwent weekly evaluations using the Basso, Beattie, Bresnahan (BBB) locomotor rating scale index, inclined plane, and OpenField test starting one week before the lesion and continuing for eight weeks. After this period, the animals were sacrificed and their spinal cords were explanted and prepared for histological analysis (hematoxylin–eosin) and immunohistochemistry for NeuN, β-III-tubulin, synaptophysin, and Caspase 3. Finally, NeuN-positive neuronal nuclei were quantified through stereology; fluorescence signal intensities for β-tubulin, synaptophyin, and Caspase 3 were quantified using an epifluorescence microscope. The injury + stim group showed significant improvement on the BBB scale compared with the injured group after the 5th week (p < 0.05). Stereological analysis showed a significantly higher average count of neural cells in the injury + stim group in relation to the injury group (1783 ± 2 vs. 897 ± 3, p < 0.001). Additionally, fluorescence signal intensity for synaptophysin was significantly higher in the injury + stim group in relation to the injury group (1294 ± 46 vs. 1198 ± 23, p < 0.01); no statistically significant difference was found in β-III-tubulin signal intensity. Finally, Caspase 3 signal intensity was significantly lower in the stim group (727 ± 123) compared with the injury group (1225 ± 87 p < 0.05), approaching levels observed in the sham and control groups. Our data suggest a regenerative and protective effect of epidural electrical stimulation in rats subjected to impact-induced traumatic spinal cord injury. Full article
(This article belongs to the Special Issue Molecular Research in Spinal Cord Injury)
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Review

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14 pages, 1134 KiB  
Review
Therapeutic Transplantation of Human Central Nervous System Organoids for Neural Reconstruction
by Sung Jun Hong, Minsung Bock, Songzi Zhang, Seong Bae An and Inbo Han
Int. J. Mol. Sci. 2024, 25(15), 8540; https://doi.org/10.3390/ijms25158540 - 5 Aug 2024
Viewed by 1572
Abstract
Damage to the central nervous system (CNS) often leads to irreversible neurological deficits, and there are currently few effective treatments available. However, recent advancements in regenerative medicine have identified CNS organoids as promising therapeutic options for addressing CNS injuries. These organoids, composed of [...] Read more.
Damage to the central nervous system (CNS) often leads to irreversible neurological deficits, and there are currently few effective treatments available. However, recent advancements in regenerative medicine have identified CNS organoids as promising therapeutic options for addressing CNS injuries. These organoids, composed of various neurons and supporting cells, have shown potential for direct repair at injury sites. CNS organoids resemble the structure and function of actual brain tissue, which allows them to adapt and function well within the physiological environment when transplanted into injury sites. Research findings suggest that CNS organoids can replace damaged neurons, form new neural connections, and promote neural recovery. This review highlights the emerging benefits, evaluates preclinical transplantation outcomes, and explores future strategies for optimizing neuroregeneration using CNS organoids. With continued research and technological advancements, these organoids could provide new hope for patients suffering from neurological deficits. Full article
(This article belongs to the Special Issue Molecular Research in Spinal Cord Injury)
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