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Neuroprotection and Repair after Spinal Cord Injury
Published in Jacques Corcos, Gilles Karsenty, Thomas Kessler, David Ginsberg, Essentials of the Adult Neurogenic Bladder, 2020
Recent evidence may indicate that the glial scar also provides some important beneficial functions after injury. Targeted depletion of reactive astrocytes that undergo mitosis indicated that after injury, this component of the glial scar serves to repair the blood-brain barrier, prevent an overwhelming inflammatory response, and limit cellular degeneration.45,46 The role of the glial scar may also be to seclude the injury site from healthy tissue, preventing spreading tissue damage.46
Transforming Growth Factor-β and CNS Scarring
Published in Martin Berry, Ann Logan, CNS Injuries: Cellular Responses and Pharmacological Strategies, 2019
Penetrating injuries of the CNS initiate a complex cellular wounding response comprising sequential and overlapping events. Acute haemorrhage and inflammation is associated with neuron degeneration; this is followed by glial/collagen scar formation, which is accompanied by an abortive regeneration response by axotomised but still viable neurons.1–3 The cellular events that culminate in glial scar formation are complex and are summarised in Figure 8.1. Whilst this figure illustrates the process of scar formation in the brain, the cellular events shown are representative of those that occur throughout the CNS.
In vivo reprogramming
Published in Christine Hauskeller, Arne Manzeschke, Anja Pichl, The Matrix of Stem Cell Research, 2019
The targeting of proliferative glial cells is another important advantage of in vivo conversion. However, it has been well documented that a wide range of somatic cells can be converted to neurons, but cells with self-renewal potency are considered to be the ideal source for therapeutic approaches. Activation of glial cells and resulting glial scar formation is associated with many neurological disorders including AD, PD, and CNS injuries such as spinal cord injury. Interestingly, the administration of reprogramming factors could effectively convert activated glial cells to functional neurons in animal models of AD (Guo et al., 2014), PD (Di Val Cervo et al., 2017), and spinal cord injury (Su et al., 2014). The successful in vivo conversion of reactive glial cells to neurons may have a significant impact on the treatment of neurodegenerative diseases in the future.
Association of beta-2-microglobulin, cystatin C and lipocalin-2 with stroke risk in the general Chinese population
Published in Annals of Medicine, 2023
Juanying Zhen, Shuyun Liu, Ryan Yan Lam Kam, Guoru Zhao, Hao Peng, Jianguo Liang, Aimin Xu, Chao Li, Lijie Ren, Jun Wu, Bernard Man Yung Cheung
The possible pathophysiological mechanisms between these three renal biomarkers and stroke have been reported previously. B2M stabilized the surface expression of MHC-I and other members of the MHC-I family, which play an important role in both the innate and adaptive immune systems [31]. As a trigger for the inflammatory process, B2M is related to atherosclerosis, which underlies the development of stroke [32,33]. Cystatin C has a direct effect on the balance of extracellular matrix proteins interacting with vessel wall remodelling [34]. High cystatin C concentration was found to be involved in inflammation, which promotes atherosclerosis [35]. LCN-2 may contribute to the development of atherosclerotic plaques by interacting with matrix metalloproteinase-9 [36]. Our previous study found that the accumulation of deamidated lipocalin-2 in arteries caused vascular inflammation and endothelial dysfunction, which are key processes in the development of stroke [37]. LCN-2 and B2M correlate with oxidative stress [38,39], which plays an important role in the pathogenesis of ischaemic stroke. The cellular effects of oxidative stress in ischaemic stroke include lipid peroxidation, protein denaturation, inactivation of enzymes, nucleic acid and DNA damage, which lead to neuronal damage and neuronal death [40]. Glial scar formation could be detected after stroke [41]. These findings provide a pathophysiological basis for the association of these three biomarkers with stroke.
Dexmedetomidine postconditioning alleviates spinal cord ischemia-reperfusion injury in rats via inhibiting neutrophil infiltration, microglia activation, reactive gliosis and CXCL13/CXCR5 axis activation
Published in International Journal of Neuroscience, 2023
Fengshou Chen, Dan Wang, Yanhua Jiang, Hong Ma, Xiaoqian Li, He Wang
Astrocytes play an important role in the mechanism of delayed onset motor dysfunction in spinal cord I/R injury as one kind of Inflammatory cells [52]. After CNS ischemia, reactive astrocytes released inflammatory cytokines, free radicals, and glutamate, resulting in nerve cell injury [19,54]. Reactive astrocytes were important in regulating neuronal cell death after CNS ischemia [19,55]. The response of the adult mammalian CNS to injury resulted in a gliosis in the lesion and the formation of a glial scar [56]. Glial scar resulted in a physical and biochemical barrier of axon regeneration, and thus affected neurologic functional recovery after CNS injury [57,58]. Attenuation of reactive astrocytes promoted function recovery after spinal cord [59,60]. In our study, we found that GFAP immunoreactivity was significantly elevated at 24 h after spinal cord I/R injury. And the increase of GFAP immunoreactivity was reduced by DEX postconditioning, which was consistent with the treatment effects of DEX in an experimental model of fibromyalgia [20]. The neuroprotective effects might be due to the reduction of inflammatory cytokines release via attenuation of reactive astrocytes. The medium DEX postconditioning significantly reduced GFAP immunoreactivity than other two doses of DEX postconditioning.
Implantation of nanofibrous silk scaffolds seeded with bone marrow stromal cells promotes spinal cord regeneration (6686 words)
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2021
Xin-Hong Wang, Xiao-Chen Tang, Xia Li, Jian-Zhong Qin, Wen-Tao Zhong, Peng Wu, Feng Zhang, Yi-Xin Shen, Ting-Ting Dai
We have previously reported our experience of a three-dimensional SF scaffold with a nanofibrous structure in which improved cell adhesion and proliferation were observed [35]. In the present study, this nanofibrous SF scaffold was optimised for cell growth, seeded with BMSCs prior to transplantation into a Sprague-Dawley (SD) rat model of SCI. We found that the BMSCs adhered well to the SF scaffold and proliferated in vitro in scaffolds both with and without the nanofibrous structure. Rats in which BMSC-seeded nanofibrous SF scaffolds were implanted displayed a higher expression of neurofilament (NF-200) and a lower expression of the glial cell marker glial fibrillary acidic protein (GFAP) than those that received a non-nanofibrous BMSC-seeded SF scaffold. NF-200 is principally located in the axon and only rarely within the cell body. It plays an important role in neuronal differentiation, axonal regeneration, and the plasticity of neural structure and function. Glial scars are considered a physical barrier preventing the regeneration of nerve fibres growing into damaged tissue. Rats treated with BMSC-seeded nanofibrous SF scaffolds also displayed superior hindlimb movement, as the Basso, Beattie, and Bresnahan (BBB) scores suggest. Therefore, nanofibrous SF scaffolds combined with BMSCs represent a promising strategy for SCI.