Regeneration and Repair in the Central Nervous System

A special issue of Bioengineering (ISSN 2306-5354). This special issue belongs to the section "Regenerative Engineering".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 3655

Special Issue Editors


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Guest Editor
Department of Bioengineering, Drug Design, Development & Delivery (4Ds) Laboratory, Clemson University, Clemson, SC 29634, USA
Interests: nanotechnology; biomaterials; drug delivery; gene therapy; regenerative medicine; tissue engineering; spinal cord injury; traumatic brain injury; neurodegenerative diseases

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Guest Editor
Department of Neurobiology & Anatomy, Marion Murray Spinal Cord Research Center, College of Medicine, Drexel University, Philadelphia, PA 19129, USA
Interests: spinal cord injury; neuropathic pain; neuroplasticity; neuroimmune interactions; neurorehabilitation; functional recovery

Special Issue Information

Dear Colleagues, 

Due to the limited intrinsic healing capacity of the adult CNS, neurotrauma in the form of traumatic brain injury (TBI), spinal cord injury (SCI), and stroke often results in permanent loss of motor, sensory, and/or cognitive function with devastating effects on an individual’s quality of life and a huge socioeconomic cost. In addition to the initial injury, neurotrauma also elicits a complex secondary injury pathophysiology including ischemia, excitotoxicity, and inflammation that lead to further neuronal and glial cell death, demyelination, and cystic cavity formation, creating multiple barriers to functional recovery. Furthermore, the capacity of spared and surviving axons for plasticity and growth is severely limited by growth inhibitors in CNS myelin and chondroitin sulfate proteoglycans (CSPGs) in the glial scar, as well as age-related and injury-induced deficiencies in intrinsic neuronal biochemistry. Although many of our colleagues have demonstrated that CNS axons can regenerate when provided with the appropriate environment or biochemical stimulation, there is no therapeutic intervention for neurotrauma that can effectively promote CNS regeneration and repair.

This Special Issue is open to original research articles, reviews, and communications that describe strategies for improving therapeutic interventions including drug delivery, gene therapy, exosome and cell therapy, nanotechnology, and tissue engineering approaches aimed at regeneration and repair after traumatic CNS trauma.

Dr. Jeoung Soo Lee
Prof. Dr. Megan Ryan Detloff
Guest Editors

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Keywords

  • traumatic brain injury
  • traumatic spinal cord injury
  • regeneration
  • neuroinflammation
  • drug delivery
  • gene therapy
  • exosome
  • cell therapy
  • nanotechnology
  • biomaterials
  • tissue engineering

Published Papers (2 papers)

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Research

20 pages, 4383 KiB  
Article
Effects of a Subanesthetic Ketamine Infusion on Inflammatory and Behavioral Outcomes after Closed Head Injury in Rats
by Haley F. Spencer, Martin Boese, Rina Y. Berman, Kennett D. Radford and Kwang H. Choi
Bioengineering 2023, 10(8), 941; https://doi.org/10.3390/bioengineering10080941 - 8 Aug 2023
Cited by 1 | Viewed by 1495
Abstract
Traumatic brain injury (TBI) affects millions of people annually, and most cases are classified as mild TBI (mTBI). Ketamine is a potent trauma analgesic and anesthetic with anti-inflammatory properties. However, ketamine’s effects on post-mTBI outcomes are not well characterized. For the current study, [...] Read more.
Traumatic brain injury (TBI) affects millions of people annually, and most cases are classified as mild TBI (mTBI). Ketamine is a potent trauma analgesic and anesthetic with anti-inflammatory properties. However, ketamine’s effects on post-mTBI outcomes are not well characterized. For the current study, we used the Closed-Head Impact Model of Engineered Rotational Acceleration (CHIMERA), which replicates the biomechanics of a closed-head impact with resulting free head movement. Adult male Sprague–Dawley rats sustained a single-session, repeated-impacts CHIMERA injury. An hour after the injury, rats received an intravenous ketamine infusion (0, 10, or 20 mg/kg, 2 h period), during which locomotor activity was monitored. Catheter blood samples were collected at 1, 3, 5, and 24 h after the CHIMERA injury for plasma cytokine assays. Behavioral assays were conducted on post-injury days (PID) 1 to 4 and included rotarod, locomotor activity, acoustic startle reflex (ASR), and pre-pulse inhibition (PPI). Brain tissue samples were collected at PID 4 and processed for GFAP (astrocytes), Iba-1 (microglia), and silver staining (axonal injury). Ketamine dose-dependently altered locomotor activity during the infusion and reduced KC/GRO, TNF-α, and IL-1β levels after the infusion. CHIMERA produced a delayed deficit in rotarod performance (PID 3) and significant axonal damage in the optic tract (PID 4), without significant changes in other behavioral or histological measures. Notably, subanesthetic doses of intravenous ketamine infusion after mTBI did not produce adverse effects on behavioral outcomes in PID 1–4 or neuroinflammation on PID 4. A further study is warranted to thoroughly investigate beneficial effects of IV ketamine on mTBI given multi-modal properties of ketamine in traumatic injury and stress. Full article
(This article belongs to the Special Issue Regeneration and Repair in the Central Nervous System)
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25 pages, 5943 KiB  
Article
Attenuation of SCI-Induced Hypersensitivity by Intensive Locomotor Training and Recombinant GABAergic Cells
by Stanislava Jergova, Elizabeth A. Dugan and Jacqueline Sagen
Bioengineering 2023, 10(1), 84; https://doi.org/10.3390/bioengineering10010084 - 9 Jan 2023
Viewed by 1587
Abstract
The underlying mechanisms of spinal cord injury (SCI)-induced chronic pain involve dysfunctional GABAergic signaling and enhanced NMDA signaling. Our previous studies showed that SCI hypersensitivity in rats can be attenuated by recombinant rat GABAergic cells releasing NMDA blocker serine-histogranin (SHG) and by intensive [...] Read more.
The underlying mechanisms of spinal cord injury (SCI)-induced chronic pain involve dysfunctional GABAergic signaling and enhanced NMDA signaling. Our previous studies showed that SCI hypersensitivity in rats can be attenuated by recombinant rat GABAergic cells releasing NMDA blocker serine-histogranin (SHG) and by intensive locomotor training (ILT). The current study combines these approaches and evaluates their analgesic effects on a model of SCI pain in rats. Cells were grafted into the spinal cord at 4 weeks post-SCI to target the chronic pain, and ILT was initiated 5 weeks post-SCI. The hypersensitivity was evaluated weekly, which was followed by histological and biochemical assays. Prolonged effects of the treatment were evaluated in subgroups of animals after we discontinued ILT. The results show attenuation of tactile, heat and cold hypersensitivity in all of the treated animals and reduced levels of proinflammatory cytokines IL1β and TNFα in the spinal tissue and CSF. Animals with recombinant grafts and ILT showed the preservation of analgesic effects even during sedentary periods when the ILT was discontinued. Retraining helped to re-establish the effect of long-term training in all of the groups, with the greatest impact being in animals with recombinant grafts. These findings suggest that intermittent training in combination with cell therapy might be an efficient approach to manage chronic pain in SCI patients. Full article
(This article belongs to the Special Issue Regeneration and Repair in the Central Nervous System)
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