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Cells
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Glial Scar: Formation and Regeneration
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Glial Scar: Formation and Regeneration

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: 30 April 2024 | Viewed by 14974

Special Issue Editors

Dr. Joanna Sypecka

E-Mail Website
Guest Editor
NeuroRepair Department, Mossakowski Medical Research Institute, Polish Academy of Sciences, Warsaw, Poland
Interests: NG2-positive progenitors; oligodendrocytes; myelinogenesis; astrocytes; microglia polarization; neuroreparative strategies
Dr. Francesca Boscia

E-Mail Website1 Website2 Website3
Guest Editor
Department of Neuroscience, Reproductive and Dentistry Sciences, Division of Pharmacology, School of Medicine, “Federico II” University of Naples, Via Pansini 5, 80131 Naples, Italy
Interests: glial cell biology; neuron-glia crosstalk; ion channels and transporters; neurodegeneration; myelin repair; demyelinating diseases
Dr. Justyna Janowska

E-Mail Website
Guest Editor
NeuroRepair Department, Mossakowski Medical Research Institute, Polish Academy of Sciences, Warsaw, Poland
Interests: glial cells; neonatal brain injuries; HIF-1 signaling; autophagy; neuroregeneration; microscopy

Special Issue Information

Dear Colleagues,

Glial scar formation is a pathological feature shared by neurodegenerative CNS diseases, i.e., MS, PD, AD, and ALS. Glial scar formation, triggered by injuries to the nervous tissue, is associated with reactive gliosis, increased cell migration, and the expression of numerous active factors (such as interleukins, trophic factors, and extracellular matrix components). Thus, this multidimensional structure comprises multiple cellular and extracellular components secreted by the activated cells. It is formed predominantly by astrocytes, oligodendrocyte progenitors, and microglia/macrophages playing roles both in the immunomodulation and in the deposition (secretion) of scar components. On the one hand, glial scars are considered to exert beneficial effects associated with the limited spread of injury, but on the other hand, it is a hindrance to tissue regeneration.

Glial scar formation: Does it exert beneficial or detrimental effects on injury spread and tissue regeneration? This question will be addressed and discussed in many respects. This Special Issue aims to provide an overview of novel discoveries in the field of glial scar formation, its structure and composition, as well as proposed innovative strategies designed to promote tissue regeneration and restoration of its functions.

Dr. Joanna Sypecka
Dr. Francesca Boscia
Dr. Justyna Janowska
Guest Editors

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. Cells 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 2700 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

  • CNS
  • reactive gliosis
  • inflammation
  • scarring
  • tissue cytoarchitecture
  • neurorepair

Published Papers (6 papers)

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Research

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17 pages, 5310 KiB  
Article
Agomir-331 Suppresses Reactive Gliosis and Neuroinflammation after Traumatic Brain Injury
by Jin-Xing Wang, Xiao Xiao, Xuan-Cheng He, Bao-Dong He, Chang-Mei Liu and Zhao-Qian Teng
Cells 2023, 12(20), 2429; https://doi.org/10.3390/cells12202429 - 11 Oct 2023
Cited by 1 | Viewed by 924
Abstract
Traumatic brain injury usually triggers glial scar formation, neuroinflammation, and neurodegeneration. However, the molecular mechanisms underlying these pathological features are largely unknown. Using a mouse model of hippocampal stab injury (HSI), we observed that miR-331, a brain-enriched microRNA, was significantly downregulated in the [...] Read more.
Traumatic brain injury usually triggers glial scar formation, neuroinflammation, and neurodegeneration. However, the molecular mechanisms underlying these pathological features are largely unknown. Using a mouse model of hippocampal stab injury (HSI), we observed that miR-331, a brain-enriched microRNA, was significantly downregulated in the early stage (0–7 days) of HSI. Intranasal administration of agomir-331, an upgraded product of miR-331 mimics, suppressed reactive gliosis and neuronal apoptosis and improved cognitive function in HSI mice. Finally, we identified IL-1β as a direct downstream target of miR-331, and agomir-331 treatment significantly reduced IL-1β levels in the hippocampus after acute injury. Our findings highlight, for the first time, agomir-331 as a pivotal neuroprotective agent for early rehabilitation of HSI. Full article
(This article belongs to the Special Issue Glial Scar: Formation and Regeneration)
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14 pages, 9359 KiB  
Article
Contribution of Oligodendrocytes, Microglia, and Astrocytes to Myelin Debris Uptake in an Explant Model of Inflammatory Demyelination in Rats
by Mariarosaria Cammarota and Francesca Boscia
Cells 2023, 12(17), 2203; https://doi.org/10.3390/cells12172203 - 03 Sep 2023
Viewed by 1544
Abstract
The internalization and degradation of myelin in glia contributes to the resolution of neuroinflammation and influences disease progression. The identification of a three-dimensional experimental model to study myelin processing under neuroinflammation will offer a novel approach for studying treatment strategies favoring inflammation resolution [...] Read more.
The internalization and degradation of myelin in glia contributes to the resolution of neuroinflammation and influences disease progression. The identification of a three-dimensional experimental model to study myelin processing under neuroinflammation will offer a novel approach for studying treatment strategies favoring inflammation resolution and neuroprotection. Here, by using a model of neuroinflammation in hippocampal explants, we show that myelin debris accumulated immediately after insult and declined at 3 days, a time point at which tentative repair processes were observed. Olig2+ oligodendrocytes upregulated the LRP1 receptor and progressively increased MBP immunoreactivity both at peri-membrane sites and within the cytosol. Oligodendrocyte NG2+ precursors increased in number and immunoreactivity one day after insult, and moderately internalized MBP particles. Three days after insult MBP was intensely coexpressed by microglia and, to a much lesser extent, by astrocytes. The engulfment of both MBP+ debris and whole MBP+ cells contributed to the greatest microglia response. In addition to improving our understanding of the spatial-temporal contribution of glial scarring to myelin uptake under neuroinflammation, our findings suggest that the exposure of hippocampal explants to LPS + IFN-γ-induced neuroinflammation may represent a valuable demyelination model for studying both the extrinsic and intrinsic myelin processing by glia under neuroinflammation. Full article
(This article belongs to the Special Issue Glial Scar: Formation and Regeneration)
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21 pages, 20157 KiB  
Article
Up-Regulation of Astrocytic Fgfr4 Expression in Adult Mice after Spinal Cord Injury
by Claire Mathilde Bringuier, Harun Najib Noristani, Jean-Christophe Perez, Maida Cardoso, Christophe Goze-Bac, Yannick Nicolas Gerber and Florence Evelyne Perrin
Cells 2023, 12(4), 528; https://doi.org/10.3390/cells12040528 - 06 Feb 2023
Cited by 2 | Viewed by 1460
Abstract
Spinal cord injury (SCI) leads to persistent neurological deficits without available curative treatment. After SCI astrocytes within the lesion vicinity become reactive, these undergo major morphological, and molecular transformations. Previously, we reported that following SCI, over 10% of resident astrocytes surrounding the lesion [...] Read more.
Spinal cord injury (SCI) leads to persistent neurological deficits without available curative treatment. After SCI astrocytes within the lesion vicinity become reactive, these undergo major morphological, and molecular transformations. Previously, we reported that following SCI, over 10% of resident astrocytes surrounding the lesion spontaneously transdifferentiate towards a neuronal phenotype. Moreover, this conversion is associated with an increased expression of fibroblast growth factor receptor 4 (Fgfr4), a neural stem cell marker, in astrocytes. Here, we evaluate the therapeutic potential of gene therapy upon Fgfr4 over-expression in mature astrocytes following SCI in adult mice. We found that Fgfr4 over-expression in astrocytes immediately after SCI improves motor function recovery; however, it may display sexual dimorphism. Improved functional recovery is associated with a decrease in spinal cord lesion volume and reduced glial reactivity. Cell-specific transcriptomic profiling revealed concomitant downregulation of Notch signaling, and up-regulation of neurogenic pathways in converting astrocytes. Our findings suggest that gene therapy targeting Fgfr4 over-expression in astrocytes after injury is a feasible therapeutic approach to improve recovery following traumatism of the spinal cord. Moreover, we stress that a sex-dependent response to astrocytic modulation should be considered for the development of effective translational strategies in other neurological disorders. Full article
(This article belongs to the Special Issue Glial Scar: Formation and Regeneration)
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Review

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26 pages, 1453 KiB  
Review
Astroglial Cells: Emerging Therapeutic Targets in the Management of Traumatic Brain Injury
by Wojciech Czyżewski, Marek Mazurek, Leon Sakwa, Michał Szymoniuk, Jennifer Pham, Barbara Pasierb, Jakub Litak, Ewa Czyżewska, Michał Turek, Bartłomiej Piotrowski, Kamil Torres and Radosław Rola
Cells 2024, 13(2), 148; https://doi.org/10.3390/cells13020148 - 12 Jan 2024
Cited by 1 | Viewed by 1464
Abstract
Traumatic Brain Injury (TBI) represents a significant health concern, necessitating advanced therapeutic interventions. This detailed review explores the critical roles of astrocytes, key cellular constituents of the central nervous system (CNS), in both the pathophysiology and possible rehabilitation of TBI. Following injury, astrocytes [...] Read more.
Traumatic Brain Injury (TBI) represents a significant health concern, necessitating advanced therapeutic interventions. This detailed review explores the critical roles of astrocytes, key cellular constituents of the central nervous system (CNS), in both the pathophysiology and possible rehabilitation of TBI. Following injury, astrocytes exhibit reactive transformations, differentiating into pro-inflammatory (A1) and neuroprotective (A2) phenotypes. This paper elucidates the interactions of astrocytes with neurons, their role in neuroinflammation, and the potential for their therapeutic exploitation. Emphasized strategies encompass the utilization of endocannabinoid and calcium signaling pathways, hormone-based treatments like 17β-estradiol, biological therapies employing anti-HBGB1 monoclonal antibodies, gene therapy targeting Connexin 43, and the innovative technique of astrocyte transplantation as a means to repair damaged neural tissues. Full article
(This article belongs to the Special Issue Glial Scar: Formation and Regeneration)
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17 pages, 1391 KiB  
Review
Understanding the Role of the Glial Scar through the Depletion of Glial Cells after Spinal Cord Injury
by Lucila Perez-Gianmarco and Maria Kukley
Cells 2023, 12(14), 1842; https://doi.org/10.3390/cells12141842 - 13 Jul 2023
Cited by 1 | Viewed by 1578
Abstract
Spinal cord injury (SCI) is a condition that affects between 8.8 and 246 people in a million and, unlike many other neurological disorders, it affects mostly young people, causing deficits in sensory, motor, and autonomic functions. Promoting the regrowth of axons is one [...] Read more.
Spinal cord injury (SCI) is a condition that affects between 8.8 and 246 people in a million and, unlike many other neurological disorders, it affects mostly young people, causing deficits in sensory, motor, and autonomic functions. Promoting the regrowth of axons is one of the most important goals for the neurological recovery of patients after SCI, but it is also one of the most challenging goals. A key event after SCI is the formation of a glial scar around the lesion core, mainly comprised of astrocytes, NG2+-glia, and microglia. Traditionally, the glial scar has been regarded as detrimental to recovery because it may act as a physical barrier to axon regrowth and release various inhibitory factors. However, more and more evidence now suggests that the glial scar is beneficial for the surrounding spared tissue after SCI. Here, we review experimental studies that used genetic and pharmacological approaches to ablate specific populations of glial cells in rodent models of SCI in order to understand their functional role. The studies showed that ablation of either astrocytes, NG2+-glia, or microglia might result in disorganization of the glial scar, increased inflammation, extended tissue degeneration, and impaired recovery after SCI. Hence, glial cells and glial scars appear as important beneficial players after SCI. Full article
(This article belongs to the Special Issue Glial Scar: Formation and Regeneration)
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20 pages, 1519 KiB  
Review
Current Advancements in Spinal Cord Injury Research—Glial Scar Formation and Neural Regeneration
by Tanner Clifford, Zachary Finkel, Brianna Rodriguez, Adelina Joseph and Li Cai
Cells 2023, 12(6), 853; https://doi.org/10.3390/cells12060853 - 09 Mar 2023
Cited by 23 | Viewed by 5402
Abstract
Spinal cord injury (SCI) is a complex tissue injury resulting in permanent and degenerating damage to the central nervous system (CNS). Detrimental cellular processes occur after SCI, including axonal degeneration, neuronal loss, neuroinflammation, reactive gliosis, and scar formation. The glial scar border forms [...] Read more.
Spinal cord injury (SCI) is a complex tissue injury resulting in permanent and degenerating damage to the central nervous system (CNS). Detrimental cellular processes occur after SCI, including axonal degeneration, neuronal loss, neuroinflammation, reactive gliosis, and scar formation. The glial scar border forms to segregate the neural lesion and isolate spreading inflammation, reactive oxygen species, and excitotoxicity at the injury epicenter to preserve surrounding healthy tissue. The scar border is a physicochemical barrier composed of elongated astrocytes, fibroblasts, and microglia secreting chondroitin sulfate proteoglycans, collogen, and the dense extra-cellular matrix. While this physiological response preserves viable neural tissue, it is also detrimental to regeneration. To overcome negative outcomes associated with scar formation, therapeutic strategies have been developed: the prevention of scar formation, the resolution of the developed scar, cell transplantation into the lesion, and endogenous cell reprogramming. This review focuses on cellular/molecular aspects of glial scar formation, and discusses advantages and disadvantages of strategies to promote regeneration after SCI. Full article
(This article belongs to the Special Issue Glial Scar: Formation and Regeneration)
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