Spinal Cord Injury and Repair: Drug Targets and Treatments

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 4621

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Guest Editor
Department of Applied Chemistry, Chaoyang University of Technology, Taichung 413310, Taiwan
Interests: spinal cord injury; neuroprotection; extracellular vesicles; phytomedicine; regenerative medicine; post-operative pain
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Special Issue Information

Dear Colleagues,

Spinal cord injury (SCI) has been a major cause of patient suffering and financial burden. The identification of drug targets for spinal cord injury and means to act on these targets have greatly accelerated progress towards functional recovery after trauma. Efforts have been directed towards the molecular characterization of spinal cord injury drug targets using many in vitro and in vivo injury models. High-throughput methods as well as structure-sensitive studies have significantly expanded the repertoire of potential targets. These provide valuable information for treatment at acute and chronic stages of the injury. Therapies aimed at many aspects of spinal cord injury including secondary inflammation, glial scarring, neuroprotection, replenishment of stem cells and cytokines, and bridging with permissive molecules may show some progress. Some of the treatments involve agents that are endogenous but reduced after injury; others are exogenous and are derived from natural sources. This Special Issue of Biomedicines focuses on recent advances in the characterization, translation, and clinical application of spinal cord injury treatment targets as well as agents that act on the targets. The goal is to encourage research and clinical strategies which, to date, are still less than satisfactory, in the hope to improve the quality of life of SCI patients.

Dr. Meng-Jen Lee
Guest Editor

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Keywords

  • spinal cord injury
  • neuroprotection
  • axon regeneration
  • targets
  • oligodendrocytes
  • macrophage
  • extracellular vesicles
  • phytomedicine
  • stem cells

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Published Papers (2 papers)

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27 pages, 9757 KiB  
Article
Exogenous FGF-1 Differently Regulates Oligodendrocyte Replenishment in an SCI Repair Model and Cultured Cells
by Meng-Jen Lee, May-Jywan Tsai, Wen-Chi Chang, Wang-Yu Hsu, Chien-Hui Hung, Ya-Tzu Chen, Tsung-Hsi Tu, Chih-Hung Shu, Ching-Jung Chen and Henrich Cheng
Biomedicines 2022, 10(11), 2724; https://doi.org/10.3390/biomedicines10112724 - 27 Oct 2022
Cited by 1 | Viewed by 1834
Abstract
We studied the phenotypes in an oligodendrocyte genesis site at the acute stage of spinal cord injury, when we observed regenerated ascending neurites. Pan-oligodendrocyte marker OLIG2+ cells were more in fibroblast growth factor (FGF)-1-treated rats (F group) than in non-treated (T group) in [...] Read more.
We studied the phenotypes in an oligodendrocyte genesis site at the acute stage of spinal cord injury, when we observed regenerated ascending neurites. Pan-oligodendrocyte marker OLIG2+ cells were more in fibroblast growth factor (FGF)-1-treated rats (F group) than in non-treated (T group) in this site, while the number of NG2+OX42− oligodendrocyte progenitor cell (OPC), CNPase+ OPC, Nkx2.2+ OPC, and APC+ remyelinating oligodendrocytes was less in the F group. Paradoxically, when we label the rats with pulsed bromodeoxyuridine (BrdU), we found that the mitotic NKX2.2+ OPC cells are more in the F group than in the T group. We tested the embryonic spinal cord mixed culture. FGF treatment resulted in more NG2(+) CNPase (+) than non-FGF-1-treated culture, while the more mature NG2(−) CNPase(+) cell numbers were reduced. When we block the FGF receptor in the injured rat model, the NG2+OX42− cell numbers were increased to be comparable to non-FGF-1 rats, while this failed to bring back the APC+ mature oligodendrocyte cell numbers. As migration of OPC toward injury is a major factor that was absent from the cell culture, we tested 8 mm away from the injury center, and found there were more NG2+ cells with FGF-1 treatment. We proposed that it was possibly a combination of migration and proliferation that resulted in a reduction in the NG2+ OPC population at the oligodendrocyte genesis site when FGF-1 was added to the spinal cord injury in vivo. Full article
(This article belongs to the Special Issue Spinal Cord Injury and Repair: Drug Targets and Treatments)
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11 pages, 426 KiB  
Case Report
Intramuscular Hematomas in Patients Receiving Prophylaxis or Anticoagulant Treatment after Spinal Cord Injury (SCI)—A Rare Complication: Description of Seven Cases and a Literature Analysis
by Magdalena Mackiewicz-Milewska, Małgorzata Cisowska-Adamiak, Iwona Szymkuć-Bukowska, Katarzyna Sakwińska, Iwona Domarecka, Anna Lewandowska and Iwona Głowacka-Mrotek
Biomedicines 2023, 11(4), 1142; https://doi.org/10.3390/biomedicines11041142 - 10 Apr 2023
Cited by 2 | Viewed by 2102
Abstract
Spinal cord injuries (SCIs) are associated with a high risk of thromboembolic complications (VTE), despite the use of antithrombotic prophylaxis in the form of low-molecular-weight heparin (LMWH). The occurrence of VTE requires, as in other diseases, full-dose antithrombotic treatment. Herein, we describe seven [...] Read more.
Spinal cord injuries (SCIs) are associated with a high risk of thromboembolic complications (VTE), despite the use of antithrombotic prophylaxis in the form of low-molecular-weight heparin (LMWH). The occurrence of VTE requires, as in other diseases, full-dose antithrombotic treatment. Herein, we describe seven cases of soft tissue hemorrhagic complications in the form of spontaneous intramuscular hematomas (SMHs) in patients after SCI undergoing rehabilitation. Four patients received anticoagulant therapy due to previously diagnosed deep vein thrombosis (DVT), and three patients received anticoagulant prophylaxis. None of the patients had a significant injury immediately before the hematoma appeared, and the only symptom was a sudden swelling of the limb without accompanying pain. The hematomas in all patients were treated conservatively. In three patients, significant decreases in hemoglobin were observed; in one patient, a blood transfusion was required for this reason. In all patients treated via anticoagulation, the anticoagulation treatment was modified at the time of diagnosis of the hematoma; in three patients, oral anticoagulants were changed to LMWH in a therapeutic dose, while in one patient, anticoagulant treatment was completely discontinued. Conclusions: Intramuscular hematomas are rare complications after SCI. Each sudden swelling of a limb requires ultrasound-based diagnostics. At the time of diagnosis of a hematoma, the level of hemoglobin and the size of the hematoma should be monitored. The treatment or anticoagulation prophylaxis should be modified if necessary. Full article
(This article belongs to the Special Issue Spinal Cord Injury and Repair: Drug Targets and Treatments)
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