Regular ArticleA Quantitative Spatial Analysis of the Blood–Spinal Cord Barrier: II. Permeability after Intraspinal Fetal Transplantation
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Exosomal miR-155 from M1-polarized macrophages promotes EndoMT and impairs mitochondrial function via activating NF-κB signaling pathway in vascular endothelial cells after traumatic spinal cord injury
2021, Redox BiologyCitation Excerpt :Spinal cord injury (SCI) is a devastating central nervous system (CNS) consequence with motor, sensory, and autonomic dysfunction. Pathophysiologically, the blood-brain barrier (BBB) or blood-spinal-cord barrier (BSCB) is ruptured after SCI, usually occurring within 5 min and lasting up to 28 days after SCI [1,2], leading to edema, inflammatory response, progressive neuron death, and glial cells activation [3]. Physiologically composed of continuous endothelial cells, pericytes, and glial cells with molecular junctions, the BSCB limits paracellular and transcellular transport in the CNS, while its dysfunction after SCI results in the infiltration of peripheral inflammatory cells and factors into the lesion and causes secondary SCI [4].
Systemic inflammation in traumatic spinal cord injury
2020, Experimental NeurologyCitation Excerpt :Systemic inflammation, either by endogenous or exogenous mediators, may promote intraspinal inflammation (Kigerl and Popovich, 2009; Schwab et al., 2014). Acutely after SCI, the blood-spinal cord barrier is breached and increased vascular permeability persists at 28 days post injury and also at eight weeks after injury (Herrera et al., 2010; Popovich et al., 1996; Schnell, 1999). Studies of the mechanisms underlying the chronic autoimmune disease, lupus, have shown that stress or infection can cause breaches in the blood brain barrier, allowing for high molecular weight mediators, such as antibodies, to gain access to the CNS, where they are neurotoxic and can alter neuronal function (Degiorgio et al., 2001; Faust et al., 2010; Kowal et al., 2004).
Proteomic analysis of the spatio-temporal based molecular kinetics of acute spinal cord injury identifies a Time-and segment-specific window for effective tissue repair
2016, Molecular and Cellular ProteomicsCitation Excerpt :The extent of microglia activation was significantly higher in gray than in white matter tracts in the caudal segments during the time period 3–7 days after injury, whereas at 10 days it dropped down. These discrepancies may be dependent on two factors: i) the metabolic changes in microglial function that are differentially affected at the gray matter necrotizing injury site and in degenerating white matter tracts, or ii) on the extent of blood-brain barrier injury, which varies between the gray and white matter (42, 47), and on the severity of injury. In this context, gray and white matters microglia express distinct morphologies and levels of cell surface antigens (48, 49), which most likely correspond with unique cell functions (50, 51).
Diffuse and persistent blood-spinal cord barrier disruption after contusive spinal cord injury rapidly recovers following intravenous infusion of bone marrow mesenchymal stem cells
2015, Experimental NeurologyCitation Excerpt :More recently, dynamic contrast-enhanced MRI in a rat model of SCI demonstrated a compromised BSCB as late as 56 days post-SCI (Cohen et al., 2009). Given the contribution of BSCB disruption to ongoing pathology in SCI, repair of the BSCB has been considered a target site for SCI therapies (Horner et al., 1996). It is well-established that intravenous injections of mesenchymal stem cells (MSCs) can improve functional recovery in experimental models of SCI (Osaka et al., 2010; Quertainmont et al., 2012).
Spinal Cord Injury and Regeneration: A Critical Evaluation of Current and Future Therapeutic Strategies
2014, Pathobiology of Human Disease: A Dynamic Encyclopedia of Disease MechanismsCell Grafting for Spinal Cord Injury Repair: Cell Replacement and Bridging Strategies
2007, Cellular Transplantation
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Present address: Laboratory of Genetics, The Salk Institute, La Jolla, CA 92186.
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Present address: The Department of Medical Microbiology & Immunology, Ohio State University, Columbus, OH 43210.