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Artykuły w czasopismach na temat „Glial scar formation”

Autor: Grafiati

Data publikacji: 30 listopada 2024

Data aktualizacji: 31 lipca 2025

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1

Perez-Gianmarco, Lucila, and Maria Kukley. "Understanding the Role of the Glial Scar through the Depletion of Glial Cells after Spinal Cord Injury." Cells 12, no. 14 (2023): 1842. http://dx.doi.org/10.3390/cells12141842.

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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 detriment

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Nicaise, Alexandra M., Andrea D’Angelo, Rosana-Bristena Ionescu, Grzegorz Krzak, Cory M. Willis, and Stefano Pluchino. "The role of neural stem cells in regulating glial scar formation and repair." Cell and Tissue Research 387, no. 3 (2021): 399–414. http://dx.doi.org/10.1007/s00441-021-03554-0.

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AbstractGlial scars are a common pathological occurrence in a variety of central nervous system (CNS) diseases and injuries. They are caused after severe damage and consist of reactive glia that form a barrier around the damaged tissue that leads to a non-permissive microenvironment which prevents proper endogenous regeneration. While there are a number of therapies that are able to address some components of disease, there are none that provide regenerative properties. Within the past decade, neural stem cells (NSCs) have been heavily studied due to their potent anti-inflammatory and reparati

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Bao, Yi, Luye Qin, Eunhee Kim, et al. "CD36 is Involved in Astrocyte Activation and Astroglial Scar Formation." Journal of Cerebral Blood Flow & Metabolism 32, no. 8 (2012): 1567–77. http://dx.doi.org/10.1038/jcbfm.2012.52.

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Inflammation is an essential component for glial scar formation. However, the upstream mediator(s) that triggers the process has not been identified. Previously, we showed that the expression of CD36, an inflammatory mediator, occurs in a subset of astcotyes in the peri-infarct area where the glial scar forms. This study investigates a role for CD36 in astrocyte activation and glial scar formation in stroke. We observed that the expression of CD36 and glial fibrillary acidic protein (GFAP) coincided in control and injured astrocytes and in the brain. Furthermore, GFAP expression was attenuated

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ZHANG, H., K. UCHIMURA, and K. KADOMATSU. "Brain Keratan Sulfate and Glial Scar Formation." Annals of the New York Academy of Sciences 1086, no. 1 (2006): 81–90. http://dx.doi.org/10.1196/annals.1377.014.

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5

Renault-Mihara, Francois, Masahiko Mukaino, Munehisa Shinozaki, et al. "Regulation of RhoA by STAT3 coordinates glial scar formation." Journal of Cell Biology 216, no. 8 (2017): 2533–50. http://dx.doi.org/10.1083/jcb.201610102.

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Understanding how the transcription factor signal transducer and activator of transcription–3 (STAT3) controls glial scar formation may have important clinical implications. We show that astrocytic STAT3 is associated with greater amounts of secreted MMP2, a crucial protease in scar formation. Moreover, we report that STAT3 inhibits the small GTPase RhoA and thereby controls actomyosin tonus, adhesion turnover, and migration of reactive astrocytes, as well as corralling of leukocytes in vitro. The inhibition of RhoA by STAT3 involves ezrin, the phosphorylation of which is reduced in STAT3-CKO

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6

Hu, Rong, Jianjun Zhou, Chunxia Luo, et al. "Glial scar and neuroregeneration: histological, functional, and magnetic resonance imaging analysis in chronic spinal cord injury." Journal of Neurosurgery: Spine 13, no. 2 (2010): 169–80. http://dx.doi.org/10.3171/2010.3.spine09190.

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Object A glial scar is thought to be responsible for halting neuroregeneration following spinal cord injury (SCI). However, little quantitative evidence has been provided to show the relationship of a glial scar and axonal regrowth after injury. Methods In this study performed in rats and dogs, a traumatic SCI model was made using a weight-drop injury device, and tissue sections were stained with H & E for immunohistochemical analysis. The function and behavior of model animals were tested using electrophysiological recording and the Basso-Beattie-Bresnahan Locomotor Rating Scale, respecti

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7

Conrad, Sabine, Hermann J. Schluesener, Mehdi Adibzahdeh, and Jan M. Schwab. "Spinal cord injury induction of lesional expression of profibrotic and angiogenic connective tissue growth factor confined to reactive astrocytes, invading fibroblasts and endothelial cells." Journal of Neurosurgery: Spine 2, no. 3 (2005): 319–26. http://dx.doi.org/10.3171/spi.2005.2.3.0319.

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Object. The glial scar composed of astrogliosis and extracellular matrix deposition represents a major impediment to axonal regeneration. The authors investigated the role of a novel profibrotic and angiogenic peptide connective tissue growth factor (CTGF [Hcs24/IGFBP-r2P]) in glial scar formation following spinal cord injury (SCI) in rats. Methods. The effects of SCI on CTGF expression during glial scar maturation 1 day to 1 month post-SCI were investigated using fluorescein-activated cell sorter (FACS) immunohistochemical analysis; these findings were compared with those obtained in sham-ope

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8

Goussev, Staci, Jung-Yu C. Hsu, Yong Lin, et al. "Differential temporal expression of matrix metalloproteinases after spinal cord injury: relationship to revascularization and wound healing." Journal of Neurosurgery: Spine 99, no. 2 (2003): 188–97. http://dx.doi.org/10.3171/spi.2003.99.2.0188.

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Object. Matrix metalloproteinases (MMPs), particularly MMP-9/gelatinase B, promote early inflammation and barrier disruption after spinal cord injury (SCI). Early blockade of MMPs after injury provides neuroprotection and improves motor outcome. There is recent evidence, however, that MMP-9 and MMP-2/gelatinase A participate in later wound healing in the injured cord. The authors therefore examined the activity of these gelatinases during revascularization and glial scar formation in the contused murine spinal cord. Methods. Gelatinase activity was evaluated using gelatin zymography 24 hours a

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9

Chen, Xuning, and Weiping Zhu. "A Mathematical Model of Regenerative Axon Growing along Glial Scar after Spinal Cord Injury." Computational and Mathematical Methods in Medicine 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/3030454.

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A major factor in the failure of central nervous system (CNS) axon regeneration is the formation of glial scar after the injury of CNS. Glial scar generates a dense barrier which the regenerative axons cannot easily pass through or by. In this paper, a mathematical model was established to explore how the regenerative axons grow along the surface of glial scar or bypass the glial scar. This mathematical model was constructed based on the spinal cord injury (SCI) repair experiments by transplanting Schwann cells as bridge over the glial scar. The Lattice Boltzmann Method (LBM) was used in this

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10

Graboviy, O. M., T. S. Mervinsky, S. I. Savosko, and L. M. Yaremenko. "Dynamics of changes in the representation of mesenchymal cells in the forming glial scar during dexamethasone application." Reports of Morphology 30, no. 3 (2024): 25–32. http://dx.doi.org/10.31393/morphology-journal-2024-30(3)-03.

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Mesenchymal stem cells are involved in cellular responses in the injured brain after a stroke. The formation of a glial scar is a local response in the brain to damage, and mesenchymal stem cells may be involved in the processes of scar formation. Mesenchymal stem cells express a range of membrane markers, the expression profile of which obviously changes as they differentiate and depends on the microenvironment in which these cells are located. However, it is still unclear where the stem cells in the damaged brain originate from – whether they come from a resident source or from the bone marr

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11

Chung, Joonho, Moon Hang Kim, Yong Je Yoon, Kil Hwan Kim, So Ra Park, and Byung Hyune Choi. "Effects of granulocyte colony–stimulating factor and granulocyte-macrophage colony–stimulating factor on glial scar formation after spinal cord injury in rats." Journal of Neurosurgery: Spine 21, no. 6 (2014): 966–73. http://dx.doi.org/10.3171/2014.8.spine131090.

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Object This study investigated the effects of granulocyte colony–stimulating factor (G-CSF) on glial scar formation after spinal cord injury (SCI) in rats and compared the therapeutic effects between G-CSF and granulocytemacrophage colony–stimulating factor (GM-CSF) to evaluate G-CSF as a potential substitute for GM-CSF in clinical application. Methods Rats were randomly assigned to 1 of 4 groups: a sham-operated group (Group 1), an SCI group without treatment (Group 2), an SCI group treated with G-CSF (Group 3), and an SCI group treated with GM-CSF (Group 4). G-CSF and GM-CSF were administere

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12

Rooney, Gemma E., Toshiki Endo, Syed Ameenuddin, et al. "Importance of the vasculature in cyst formation after spinal cord injury." Journal of Neurosurgery: Spine 11, no. 4 (2009): 432–37. http://dx.doi.org/10.3171/2009.4.spine08784.

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Object Glial scar and cystic formation greatly contribute to the inhibition of axonal regeneration after spinal cord injury (SCI). Attempts to promote axonal regeneration are extremely challenging in this type of hostile environment. The objective of this study was to examine the surgical methods that may be used to assess the factors that influence the level of scar and cystic formation in SCI. Methods In the first part of this study, a complete transection was performed at vertebral level T9–10 in adult female Sprague-Dawley rats. The dura mater was either left open (control group) or was cl

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13

Clifford, Tanner, Zachary Finkel, Brianna Rodriguez, Adelina Joseph, and Li Cai. "Current Advancements in Spinal Cord Injury Research—Glial Scar Formation and Neural Regeneration." Cells 12, no. 6 (2023): 853. http://dx.doi.org/10.3390/cells12060853.

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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 secr

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14

Liu, Jingzhou, Xin Xin, Jiejie Sun, et al. "Dual-targeting AAV9P1-mediated neuronal reprogramming in a mouse model of traumatic brain injury." Neural Regeneration Research 19, no. 3 (2023): 629–35. http://dx.doi.org/10.4103/1673-5374.380907.

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Abstract JOURNAL/nrgr/04.03/01300535-202403000-00038/inline-graphic1/v/2023-08-11T153926Z/r/image-tiff Traumatic brain injury results in neuronal loss and glial scar formation. Replenishing neurons and eliminating the consequences of glial scar formation are essential for treating traumatic brain injury. Neuronal reprogramming is a promising strategy to convert glial scars to neural tissue. However, previous studies have reported inconsistent results. In this study, an AAV9P1 vector incorporating an astrocyte-targeting P1 peptide and glial fibrillary acidic protein promoter was used to achieve

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15

Onodera, Junya, Yuji Ikegaya, and Ryuta Koyama. "Involvement of microglial TRPV4 on glial scar formation." Proceedings for Annual Meeting of The Japanese Pharmacological Society 95 (2022): 1—P—020. http://dx.doi.org/10.1254/jpssuppl.95.0_1-p-020.

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Sutin, Jerome, та Ronald Griffith. "β-Adrenergic Receptor Blockade Suppresses Glial Scar Formation". Experimental Neurology 120, № 2 (1993): 214–22. http://dx.doi.org/10.1006/exnr.1993.1056.

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Wang, Haijun, Guobin Song, Haoyu Chuang, et al. "Portrait of glial scar in neurological diseases." International Journal of Immunopathology and Pharmacology 31 (January 2018): 205873841880140. http://dx.doi.org/10.1177/2058738418801406.

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Fibrosis is formed after injury in most of the organs as a common and complex response that profoundly affects regeneration of damaged tissue. In central nervous system (CNS), glial scar grows as a major physical and chemical barrier against regeneration of neurons as it forms dense isolation and creates an inhibitory environment, resulting in limitation of optimal neural function and permanent deficits of human body. In neurological damages, glial scar is mainly attributed to the activation of resident astrocytes which surrounds the lesion core and walls off intact neurons. Glial cells induce

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18

Sofroniew, Michael V. "Molecular dissection of reactive astrogliosis and glial scar formation." Trends in Neurosciences 32, no. 12 (2009): 638–47. http://dx.doi.org/10.1016/j.tins.2009.08.002.

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Fu, Xiongjie, Yingfeng Wan, Ya Hua, Guohua Xi, and Richard F. Keep. "Characteristics of Scar Formation After Intracerebral Hemorrhage in Aged Rats: Effects of Deferoxamine." Cells 14, no. 15 (2025): 1127. https://doi.org/10.3390/cells14151127.

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Intracerebral hemorrhage (ICH), a severe stroke subtype common in the elderly, often results in high morbidity and mortality, with limited treatment options for long-term recovery. While glial scar formation is increasingly recognized as key to central nervous system (CNS) repair, its role and characteristics in the aging brain post-ICH remain unclear. This study investigated glial scar formation after ICH (100 μL autologous blood injected into the right basal ganglia model) in aged Fischer 344 rats and assessed the effects of deferoxamine (DFX) treatment. Histological and immunohistochemical

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Rodriguez-Grande, Beatriz, Matimba Swana, Loan Nguyen, et al. "The Acute-Phase Protein PTX3 is an Essential Mediator of Glial Scar Formation and Resolution of Brain Edema after Ischemic Injury." Journal of Cerebral Blood Flow & Metabolism 34, no. 3 (2013): 480–88. http://dx.doi.org/10.1038/jcbfm.2013.224.

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Acute-phase proteins (APPs) are key effectors of the immune response and are routinely used as biomarkers in cerebrovascular diseases, but their role during brain inflammation remains largely unknown. Elevated circulating levels of the acute-phase protein pentraxin-3 (PTX3) are associated with worse outcome in stroke patients. Here we show that PTX3 is expressed in neurons and glia in response to cerebral ischemia, and that the proinflammatory cytokine interleukin-1 (IL-1) is a key driver of PTX3 expression in the brain after experimental stroke. Gene deletion of PTX3 had no significant effect

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Korte, G. E., M. Marko, and G. Hageman. "High-voltage electron microscopy of subretinal scar formation." Proceedings, annual meeting, Electron Microscopy Society of America 50, no. 1 (1992): 486–87. http://dx.doi.org/10.1017/s0424820100122836.

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Sodium iodate iv. damages the retinal pigment epithelium (RPE) in rabbits. Where RPE does not regenerate (e.g., 1,2) Muller glial cells (MC) forma subretinal scar that replaces RPE. The MC response was studied by HVEM in 3D computer reconstructions of serial thick sections, made using the STEREC0N program (3), and the HVEM at the NYS Dept. of Health in Albany, NY. Tissue was processed for HVEM or immunofluorescence localization of a monoclonal antibody recognizing MG microvilli (4).

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Li, Xin, Yan Qian, Wanling Shen, et al. "Mechanism of SET8 Activates the Nrf2-KEAP1-ARE Signaling Pathway to Promote the Recovery of Motor Function after Spinal Cord Injury." Mediators of Inflammation 2023 (March 10, 2023): 1–13. http://dx.doi.org/10.1155/2023/4420592.

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Background. Spinal cord injury (SCI) is a common injury of the central nervous system (CNS), and astrocytes are relatively abundant glial cells in the CNS that impairs the recovery of motor function after SCI. It was confirmed that the oxidative stress of mitochondria leads to the accumulation of reactive oxygen species (ROS) in cells, which plays a key role in the motor function of astrocytes. However, the mechanism by which oxidative stress affects astrocyte motility after SCI is still unexplained. Therefore, this study investigated the influence of SET8-regulated oxidative stress on astrocy

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Carvalho, Juliana Casanovas de, César Augusto Abreu-Pereira, Lucas Cauê da Silva Assunção, Rosana Costa Casanovas, Ana Lucia Abreu-Silva, and Matheus Levi Tajra Feitosa. "Correlation of Nogo A release with glia scar formation in spinal cord injury." Research, Society and Development 10, no. 6 (2021): e25410615688. http://dx.doi.org/10.33448/rsd-v10i6.15688.

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Several axonal growth inhibitors have already been identified following spinal cord injury, the most known being myelin-derived proteins, such as Nogo-A. The present study aimed to correlate the formation of glial scar with the beginning of growth inhibitor, Nogo-A, release in rats previously submitted to compressive spinal cord injury. For this, 12 male and female Wistar rats (250 ± 50g) were divided into 3 groups of 4 animals each, according to the animals' euthanasia time after spinal cord injury (G3 - three days; G5 - five days; G7 - seven days). Spinal cord injuries were induced by means

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Badan, I., B. Buchhold, A. Hamm, et al. "Accelerated Glial Reactivity to Stroke in Aged Rats Correlates with Reduced Functional Recovery." Journal of Cerebral Blood Flow & Metabolism 23, no. 7 (2003): 845–54. http://dx.doi.org/10.1097/01.wcb.0000071883.63724.a7.

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Following cerebral ischemia, perilesional astrocytes and activated microglia form a glial scar that hinders the genesis of new axons and blood vessels in the infarcted region. Since glial reactivity is chronically augmented in the normal aging brain, the authors hypothesized that postischemic gliosis would be temporally abnormal in aged rats compared to young rats. Focal cerebral ischemia was produced by reversible occlusion of the right middle cerebral artery in 3- and 20-month-old male Sprague Dawley rats. The functional outcome was assessed in neurobehavioral tests at 3, 7, 14, and 28 days

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Pekny, Milos, Clas B. Johansson, Camilla Eliasson, et al. "Abnormal Reaction to Central Nervous System Injury in Mice Lacking Glial Fibrillary Acidic Protein and Vimentin." Journal of Cell Biology 145, no. 3 (1999): 503–14. http://dx.doi.org/10.1083/jcb.145.3.503.

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In response to injury of the central nervous system, astrocytes become reactive and express high levels of the intermediate filament (IF) proteins glial fibrillary acidic protein (GFAP), vimentin, and nestin. We have shown that astrocytes in mice deficient for both GFAP and vimentin (GFAP−/−vim−/−) cannot form IFs even when nestin is expressed and are thus devoid of IFs in their reactive state. Here, we have studied the reaction to injury in the central nervous system in GFAP−/−, vimentin−/−, or GFAP−/−vim−/− mice. Glial scar formation appeared normal after spinal cord or brain lesions in GFAP

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Wiemann, Susanne, Jacqueline Reinhard, and Andreas Faissner. "Immunomodulatory role of the extracellular matrix protein tenascin-C in neuroinflammation." Biochemical Society Transactions 47, no. 6 (2019): 1651–60. http://dx.doi.org/10.1042/bst20190081.

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The extracellular matrix (ECM) consists of a dynamic network of various macromolecules that are synthesized and released by surrounding cells into the intercellular space. Glycoproteins, proteoglycans and fibrillar proteins are main components of the ECM. In addition to general functions such as structure and stability, the ECM controls several cellular signaling pathways. In this context, ECM molecules have a profound influence on intracellular signaling as receptor-, adhesion- and adaptor-proteins. Due to its various functions, the ECM is essential in the healthy organism, but also under pat

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Huang, Lijie, Zhe-Bao Wu, Qichuan ZhuGe, et al. "Glial Scar Formation Occurs in the Human Brain after Ischemic Stroke." International Journal of Medical Sciences 11, no. 4 (2014): 344–48. http://dx.doi.org/10.7150/ijms.8140.

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Beach, Krista M., Jianbo Wang, and Deborah C. Otteson. "Regulation of Stem Cell Properties of Müller Glia by JAK/STAT and MAPK Signaling in the Mammalian Retina." Stem Cells International 2017 (2017): 1–15. http://dx.doi.org/10.1155/2017/1610691.

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In humans and other mammals, the neural retina does not spontaneously regenerate, and damage to the retina that kills retinal neurons results in permanent blindness. In contrast to embryonic stem cells, induced pluripotent stem cells, and embryonic/fetal retinal stem cells, Müller glia offer an intrinsic cellular source for regenerative strategies in the retina. Müller glia are radial glial cells within the retina that maintain retinal homeostasis, buffer ion flux associated with phototransduction, and form the blood/retinal barrier within the retina proper. In injured or degenerating retinas,

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Otte, Elisabeth, Andreas Vlachos, and Maria Asplund. "Engineering strategies towards overcoming bleeding and glial scar formation around neural probes." Cell and Tissue Research 387, no. 3 (2022): 461–77. http://dx.doi.org/10.1007/s00441-021-03567-9.

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AbstractNeural probes are sophisticated electrophysiological tools used for intra-cortical recording and stimulation. These microelectrode arrays, designed to penetrate and interface the brain from within, contribute at the forefront of basic and clinical neuroscience. However, one of the challenges and currently most significant limitations is their ‘seamless’ long-term integration into the surrounding brain tissue. Following implantation, which is typically accompanied by bleeding, the tissue responds with a scarring process, resulting in a gliotic region closest to the probe. This glial sca

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Li, Ping, Zhao-Qian Teng, and Chang-Mei Liu. "Extrinsic and Intrinsic Regulation of Axon Regeneration by MicroRNAs after Spinal Cord Injury." Neural Plasticity 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/1279051.

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Spinal cord injury is a devastating disease which disrupts the connections between the brain and spinal cord, often resulting in the loss of sensory and motor function below the lesion site. Most injured neurons fail to regenerate in the central nervous system after injury. Multiple intrinsic and extrinsic factors contribute to the general failure of axonal regeneration after injury. MicroRNAs can modulate multiple genes’ expression and are tightly controlled during nerve development or the injury process. Evidence has demonstrated that microRNAs and their signaling pathways play important rol

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Cloutier, Frank, Ilse Sears-Kraxberger, Krista Keachie, and Hans S. Keirstead. "Immunological Demyelination Triggers Macrophage/Microglial Cells Activation without Inducing Astrogliosis." Clinical and Developmental Immunology 2013 (2013): 1–14. http://dx.doi.org/10.1155/2013/812456.

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The glial scar formed by reactive astrocytes and axon growth inhibitors associated with myelin play important roles in the failure of axonal regeneration following central nervous system (CNS) injury. Our laboratory has previously demonstrated that immunological demyelination of the CNS facilitates regeneration of severed axons following spinal cord injury. In the present study, we evaluate whether immunological demyelination is accompanied with astrogliosis. We compared the astrogliosis and macrophage/microglial cell responses 7 days after either immunological demyelination or a stab injury t

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Saadoun, S. "Involvement of aquaporin-4 in astroglial cell migration and glial scar formation." Journal of Cell Science 118, no. 24 (2005): 5691–98. http://dx.doi.org/10.1242/jcs.02680.

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Hsu, J. Y. C., L. Y. W. Bourguignon, C. M. Adams, et al. "Matrix Metalloproteinase-9 Facilitates Glial Scar Formation in the Injured Spinal Cord." Journal of Neuroscience 28, no. 50 (2008): 13467–77. http://dx.doi.org/10.1523/jneurosci.2287-08.2008.

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Ohlsson, Marcus, Per Mattsson, Barbara D. Wamil, Carl G. Hellerqvist, and Mikael Svensson. "Macrophage stimulation using a group B-streptococcus exotoxin (CM101) leads to axonal regrowth in the injured optic nerve." Restorative Neurology and Neuroscience 22, no. 1 (2004): 33–41. https://doi.org/10.3233/rnn-2004-00244.

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Purpose: A group B-streptococcus exotoxin (CM101) was administered following optic nerve injury in adult rats in order to analyze putative effects on macrophages, glial scar formation and regrowth of axons in the lesioned optic nerve. Methods: After a standardized intraorbital optic nerve crush, animals were randomized to treatment with CM101 (30 μm/kg body weight, iv, repeated every other day) or vehicle alone. Morphology (semithin sections) and immunohistochemistry directed towards macrophages (ED1), neurofilament (NF), astrocytes (GFAP) and regenerative sprouts (GAP43) were employed at diff

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Leme, Ricardo José de Almeida, and Gerson Chadi. "Distant microglial and astroglial activation secondary to experimental spinal cord lesion." Arquivos de Neuro-Psiquiatria 59, no. 3A (2001): 483–92. http://dx.doi.org/10.1590/s0004-282x2001000400002.

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This paper analysed whether glial responses following a spinal cord lesion is restricted to a scar formation close to the wound or they might be also related to widespread paracrine trophic events in the entire cord. Spinal cord hemitransection was performed in adult rats at the thoracic level. Seven days and three months later the spinal cords were removed and submitted to immunohistochemistry of glial fibrillary acidic protein (GFAP) and OX42, markers for astrocytes and microglia, as well as of basic fibroblast growth factor (bFGF), an astroglial neurotrophic factor. Computer assisted image

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Robel, Stefanie. "Astroglial Scarring and Seizures." Neuroscientist 23, no. 2 (2016): 152–68. http://dx.doi.org/10.1177/1073858416645498.

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Epilepsy is among the most prevalent chronic neurological diseases and affects an estimated 2.2 million people in the United States alone. About one third of patients are resistant to currently available antiepileptic drugs, which are exclusively targeting neuronal function. Yet, reactive astrocytes have emerged as potential contributors to neuronal hyperexcitability and seizures. Astrocytes react to any kind of CNS insult with a range of cellular adjustments to form a scar and protect uninjured brain regions. This process changes astrocyte physiology and can affect neuronal network function i

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Yeh, Jue-Zong, Ding-Han Wang, Juin-Hong Cherng, et al. "A Collagen-Based Scaffold for Promoting Neural Plasticity in a Rat Model of Spinal Cord Injury." Polymers 12, no. 10 (2020): 2245. http://dx.doi.org/10.3390/polym12102245.

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In spinal cord injury (SCI) therapy, glial scarring formed by activated astrocytes is a primary problem that needs to be solved to enhance axonal regeneration. In this study, we developed and used a collagen scaffold for glial scar replacement to create an appropriate environment in an SCI rat model and determined whether neural plasticity can be manipulated using this approach. We used four experimental groups, as follows: SCI-collagen scaffold, SCI control, normal spinal cord-collagen scaffold, and normal control. The collagen scaffold showed excellent in vitro and in vivo biocompatibility.

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Zhao, Lina, Xianyu Zhang, and Chunhai Zhang. "Methimazole Inhibits the Expression of GFAP and the Migration of Astrocyte in Scratched Wound Model In Vitro." Mediators of Inflammation 2020 (April 13, 2020): 1–7. http://dx.doi.org/10.1155/2020/4027470.

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Astrocytes respond to central nervous system (CNS) insults with varieties of changes, such as cellular hypertrophy, migration, proliferation, scar formation, and upregulation of glial fibrillary acidic protein (GFAP) expression. While scar formation plays a very important role in wound healing and prevents further bleeding by forming a physical barrier, it is also one of key features of CNS injury, resulting in glial scar formation (astrogliosis), which is closely related to treatment resistant epilepsy, chronic pain, and other devastating diseases. Therefore, slowing the astrocytic activation

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Widayati, Aris, Fedik Abdul Rantam, Abdulloh Machin та Wibi Riawan. "Inhibition of Neurogenesis and Induction of Glial Scar Formation by Neuroinflammation Following Ischemic Stroke: Evaluation of BDNF, GFAP, HMGB1 and TNF-α Expressions". Indonesian Biomedical Journal 17, № 1 (2025): 99–108. https://doi.org/10.18585/inabj.v17i1.3439.

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BACKGROUND: Ischemic stroke remains as a major health problem and one important process in Ischemic Stroke is neuroinflammation which has a principal role to maintain the balance of neurogenesis and neurodegeneration process in the brain. Neuroinflammation can lead to glial scar and inhibit neurogenesis processes which is needed for recovery neuron function. This study was conducted to observe the role of high mobility group box 1 (HMGB1) and tumor necrosis factor-α (TNF-α) as neuroinflammation markers to glial fibrillary acidic protein (GFAP) as glial scar marker and to brain-derived neurotro

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Hayashi, Noriko, Seiji Miyata, Yutaka Kariya, Ryo Takano, Saburo Hara, and Kaeko Kamei. "Attenuation of glial scar formation in the injured rat brain by heparin oligosaccharides." Neuroscience Research 49, no. 1 (2004): 19–27. http://dx.doi.org/10.1016/j.neures.2004.01.007.

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Romero-Ramírez, Lorenzo, Manuel Nieto-Sampedro, and MAsunción Barreda-Manso. "All roads go to Salubrinal: endoplasmic reticulum stress, neuroprotection and glial scar formation." Neural Regeneration Research 10, no. 12 (2015): 1926. http://dx.doi.org/10.4103/1673-5374.169619.

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Song, Byeong Gwan, Su Yeon Kwon, Jae Won Kyung, et al. "Synaptic Cell Adhesion Molecule 3 (SynCAM3) Deletion Promotes Recovery from Spinal Cord Injury by Limiting Glial Scar Formation." International Journal of Molecular Sciences 23, no. 11 (2022): 6218. http://dx.doi.org/10.3390/ijms23116218.

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Synaptic cell adhesion molecules (SynCAMs) play an important role in the formation and maintenance of synapses and the regulation of synaptic plasticity. SynCAM3 is expressed in the synaptic cleft of the central nervous system (CNS) and is involved in the connection between axons and astrocytes. We hypothesized that SynCAM3 may be related to the astrocytic scar (glial scar, the most important factor of CNS injury treatment) through extracellular matrix (ECM) reconstitution. Thus, we investigated the influence of the selective removal of SynCAM3 on the outcomes of spinal cord injury (SCI). SynC

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Sun, Daniel, and Tatjana C. Jakobs. "Structural Remodeling of Astrocytes in the Injured CNS." Neuroscientist 18, no. 6 (2011): 567–88. http://dx.doi.org/10.1177/1073858411423441.

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Astrocytes respond to all forms of CNS insult and disease by becoming reactive, a nonspecific but highly characteristic response that involves various morphological and molecular changes. Probably the most recognized aspect of reactive astrocytes is the formation of a glial scar that impedes axon regeneration. Although the reactive phenotype was first suggested more than 100 years ago based on morphological changes, the remodeling process is not well understood. We know little about the actual structure of a reactive astrocyte, how an astrocyte remodels during the progression of an insult, and

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Parry, Phillip V., and Johnathan A. Engh. "Promotion of Neuronal Recovery Following Experimental SCI via Direct Inhibition of Glial Scar Formation." Neurosurgery 70, no. 6 (2012): N10—N11. http://dx.doi.org/10.1227/01.neu.0000414941.18107.47.

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Zhu, Yong-Ming, Xue Gao, Yong Ni, et al. "Sevoflurane postconditioning attenuates reactive astrogliosis and glial scar formation after ischemia–reperfusion brain injury." Neuroscience 356 (July 2017): 125–41. http://dx.doi.org/10.1016/j.neuroscience.2017.05.004.

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Wang, Yu-Fu, Jia-Ning Zu, Jing Li, Chao Chen, Chun-Yang Xi, and Jing-Long Yan. "Curcumin promotes the spinal cord repair via inhibition of glial scar formation and inflammation." Neuroscience Letters 560 (February 2014): 51–56. http://dx.doi.org/10.1016/j.neulet.2013.11.050.

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Uesugi, Masafumi, Yoshitoshi Kasuva, Hiroshi Hama, Tomoh Masaki, and Katsutoshi Goto. "The Participation of Endogenous ET-1 in Glial Scar formation after Spinal Cord Injury." Japanese Journal of Pharmacology 73 (1997): 112. http://dx.doi.org/10.1016/s0021-5198(19)44953-6.

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Okuda, Akinori, Noriko Horii-Hayashi, Takayo Sasagawa, et al. "Bone marrow stromal cell sheets may promote axonal regeneration and functional recovery with suppression of glial scar formation after spinal cord transection injury in rats." Journal of Neurosurgery: Spine 26, no. 3 (2017): 388–95. http://dx.doi.org/10.3171/2016.8.spine16250.

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OBJECTIVE Transplantation of bone marrow stromal cells (BMSCs) is a theoretical potential as a therapeutic strategy in the treatment of spinal cord injury (SCI). Although a scaffold is sometimes used for retaining transplanted cells in damaged tissue, it is also known to induce redundant immunoreactions during the degradation processes. In this study, the authors prepared cell sheets made of BMSCs, which are transplantable without a scaffold, and investigated their effects on axonal regeneration, glial scar formation, and functional recovery in a completely transected SCI model in rats. METHOD

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Zhang, Rongyi, Junhua Wang, Qingwen Deng, et al. "Mesenchymal Stem Cells Combined With Electroacupuncture Treatment Regulate the Subpopulation of Macrophages and Astrocytes to Facilitate Axonal Regeneration in Transected Spinal Cord." Neurospine 20, no. 4 (2023): 1358–79. http://dx.doi.org/10.14245/ns.2346824.412.

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Objective: Herein, we investigated whether mesenchymal stem cells (MSCs) transplantation combined with electroacupuncture (EA) treatment could decrease the proportion of proinflammatory microglia/macrophages and neurotoxic A1 reactive astrocytes and inhibit glial scar formation to enhance axonal regeneration after spinal cord injury (SCI).Methods: Adult rats were divided into 5 groups after complete transection of the spinal cord at the T10 level: a control group, a nonacupoint EA (NA-EA) group, an EA group, an MSC group, and an MSCs+EA group. Immunofluorescence labeling, quantitative real-tim

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Pasterkamp, R. Jeroen, and Joost Verhaagen. "Semaphorins in axon regeneration: developmental guidance molecules gone wrong?" Philosophical Transactions of the Royal Society B: Biological Sciences 361, no. 1473 (2006): 1499–511. http://dx.doi.org/10.1098/rstb.2006.1892.

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Semaphorins are developmental axon guidance cues that continue to be expressed during adulthood and are regulated by neural injury. During the formation of the nervous system, repulsive semaphorins guide axons to their targets by restricting and channelling their growth. They affect the growth cone cytoskeleton through interactions with receptor complexes that are linked to a complicated intracellular signal transduction network. Following injury, regenerating axons stop growing when they reach the border of the glial-fibrotic scar, in part because they encounter a potent molecular barrier tha

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