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Gotowe bibliografie tematyczne / Glial scar formation

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Gotowa bibliografia na temat „Glial scar formation”

Autor: Grafiati

Data publikacji: 30 listopada 2024

Data aktualizacji: 31 lipca 2025

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Artykuły w czasopismach na temat "Glial scar formation"

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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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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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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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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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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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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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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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Rozprawy doktorskie na temat "Glial scar formation"

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Manrique-Castaño, Daniel [Verfasser], Dirk Matthias [Gutachter] Hermann, Patrik [Gutachter] Krieger, and Tracy D. [Gutachter] Farr. "Influence of the extracellular matrix protein Tenascin-C in the immune response, glial scar formation and ECM reorganization following cerebral ischemia in mice / Daniel Manrique-Castaño ; Gutachter: Dirk Matthias Hermann, Patrik Krieger, Tracy D. Farr ; International Graduate School of Neuroscience." Bochum : Ruhr-Universität Bochum, 2020. http://d-nb.info/1223176096/34.

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Clain, Julien. "Impact des maladies métaboliques sur la cicatrice gliale, la plasticité cérébrale et la récupération fonctionnelle : exemple de l'accident vasculaire cérébral." Electronic Thesis or Diss., La Réunion, 2024. https://elgebar.univ-reunion.fr/login?url=http://thesesenligne.univ.run/24_13_J_CLAIN.pdf.

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L’accident vasculaire cérébral ischémique (AVCi) est une des pathologies les plus mortelles au monde. Le diabète de type II et l’obésité, qui représentent les deux maladies métaboliques les plus fréquentes, sont des facteurs de risque importants de la survenue d’un AVCi, et leur prévalence est augmentée à La Réunion. Par conséquent, le nombre d’AVCi à La Réunion par habitant est plus élevé que la moyenne nationale. Le diabète et l’obésité aggravent aussi les conséquences de l’ischémie cérébrale, via des mécanismes moléculaires et cellulaires qui ne sont pas encore élucidés. Au cours d’un AVCi,

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Części książek na temat "Glial scar formation"

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Logan, Ann, and Martin Berry. "Cellular and Molecular Determinants of Glial Scar Formation." In Advances in Experimental Medicine and Biology. Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0123-7_4.

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Frontczak-Baniewicz, Malgorzata, Lidia Strużynska, Jaroslaw Andrychowski, Jolanta Opertowska, Dorota Sulejczak, and Michal Walski. "Ultrastructural and Immunochemical Studies of Glial Scar Formation in Diabetic Rats." In Brain Edema XIV. Springer Vienna, 2009. http://dx.doi.org/10.1007/978-3-211-98811-4_47.

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Pilkinton, Sophie, T. J. Hollingsworth, Brian Jerkins, and Monica M. Jablonski. "An Overview of Glaucoma: Bidirectional Translation between Humans and Pre-Clinical Animal Models." In Animal Models in Medicine and Biology [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97145.

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Glaucoma is a multifactorial, polygenetic disease with a shared outcome of loss of retinal ganglion cells and their axons, which ultimately results in blindness. The most common risk factor of this disease is elevated intraocular pressure (IOP), although many glaucoma patients have IOPs within the normal physiological range. Throughout disease progression, glial cells in the optic nerve head respond to glaucomatous changes, resulting in glial scar formation as a reaction to injury. This chapter overviews glaucoma as it affects humans and the quest to generate animal models of glaucoma so that

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Rodrígez-Barrera, Roxana, Adrián Flores-Romero, Julián García-Sánchez, Lisset Karina Navarro-Torres, Marcela Garibay-López, and Elisa García-Vences. "Cytokines in Scar Glial Formation after an Acute and Chronic Spinal Cord Injury." In Cytokines. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.93005.

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Lucchinetti, C., and H. Lassmann. "The Neuropathology of Multiple Sclerosis." In Glial Cell Development basic principles and clinical relevance second edition. Oxford University PressOxford, 2001. http://dx.doi.org/10.1093/oso/9780198524786.003.0018.

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Abstract Multiple sclerosis (MS) is an inflammatory relapsing or progressive central nervous system (CNS) disorder characterized by focal areas of myelin destruction associated with astroglial scar formation (Figure 18.1). These lesions are scattered throughout the CNS with a predilection for the optic nerves, brainstem, spinal cord and periventricular white matter. The initial pathological descriptions of MS were reported in the first half of the 19th century (Cruveilhier, 1835; Carswell, 1838; Charcot, 1868). Later studies revealed that the classical clinico-pathological pattern of MS descri

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El-Mansoury, Bilal, Kamal Smimih, Youssef Ait Hamdan, Ahmed Draoui, Samira Boulbaroud, and Arumugam Radhakrishnan Jayakumar. "Microglial Cells Function in the Central Nervous System." In Physiology and Function of Glial Cells in Health and Disease. IGI Global, 2023. http://dx.doi.org/10.4018/978-1-6684-9675-6.ch004.

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Microglia are the resident macrophages of the central nervous system (CNS). These cells of mesodermal/mesenchymal origin migrate into all regions of the CNS. Recent studies indicate that even in the normal brain, microglia have highly motile processes by which they scan their territorial domains. By a large number of signaling pathways, they can communicate with macroglial cells (e.g. astrocytes) and neurons and with cells of the immune system. Under normal physiological conditions, microglia constantly monitor their microenvironment and survey neurons. Microglia have other functions including

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Streszczenia konferencji na temat "Glial scar formation"

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Bernick, Kristin B., and Simona Socrate. "Substrate Dependence of Mechanical Response of Neurons and Astrocytes." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53538.

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The response of neural cells to mechanical cues is a critical component of the innate neuroprotective cascade aimed at minimizing the consequences of traumatic brain injury (TBI). Reactive gliosis and the formation of glial scars around the lesion site are among the processes triggered by TBI where mechanical stimuli play a central role. It is well established that the mechanical properties of the microenvironment influence phenotype and morphology in most cell types. It has been shown that astrocytes change morphology [1] and cytoskeletal content [2] when grown on substrates of varying stiffn

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