Regular ArticleSpinal Cord Compression Injury in Guinea Pigs: Structural Changes of Endothelium and Its Perivascular Cell Associations after Blood–Brain Barrier Breakdown and Repair☆,☆☆
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2017, NeuropharmacologyImmunohistochemical detectability of cerebrovascular utrophin depends on the condition of basal lamina
2014, Neuroscience LettersOver-expression of laminin correlates to recovery of vasogenic edema following status epilepticus
2014, NeuroscienceCitation Excerpt :In contrast to dystrophin expression, laminin expression is remarkably upregulated in the BMs of vessels after SE in parallel with the astroglial loss (Biagini et al., 2008; Gualtieri et al., 2012). This laminin over-expression is explained by an improved accessibility of laminin epitopes in damaged blood vessels (Szabó and Kálmán, 2004; Kálmán et al., 2011), since the astrocytic anchoring to BMs is exposed in consequence of brain damage and inflammation (Jaeger and Blight, 1997; Kálmán et al., 2011; Gualtieri et al., 2012). Therefore, up-regulation of laminin expression is one of the consequences from BBB modification and predicts astroglial damage following SE (Gualtieri et al., 2012).
Increased perivascular laminin predicts damage to astrocytes in CA3 and piriform cortex following chemoconvulsive treatments
2012, NeuroscienceCitation Excerpt :The astrocytic end-feet are anchored to this capillary basal lamina by the so-called dystrophin–glycoprotein complex, which is linked to laminin and is crucial to BBB integrity (Abbott et al., 2006; del Zoppo et al., 2006; Wolburg et al., 2009). On the other hand, the astrocytic anchoring to capillary basal lamina is released in consequence of tissue damage and inflammation (Jaeger and Blight, 1997; Kálmán et al., 2011) or angiogenesis (Sixt et al., 2001). In view of these data, it appeared interesting to examine the relationship between the vascular changes that follow SE and glial cells, especially astrocytes.
The challenges of long-distance axon regeneration in the injured CNS
2012, Progress in Brain ResearchCitation Excerpt :Severance of posterior and anterior spinal veins and arteries that lie on the surface of the cord supplying the interior gray matter causes an ischaemic insult to the targeted segment as well as below the level of the lesion (Sandler and Tator, 1976). There is loss of the blood–brain barrier (BBB), internal hemorrhage (Jaeger and Blight, 1997; Maikos and Shreiber, 2007), altered blood flow (Senter and Venes, 1978), and endothelial cell death (Benton et al., 2008) at the site of injury. These events further prolong and exacerbate ischaemia and render the BBB permeable.
A swift expanding trend of extracellular vesicles in spinal cord injury research: a bibliometric analysis
2023, Journal of Nanobiotechnology
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Supported by the School of Veterinary Medicine, Purdue University and Public Health Service Grant RO1-NS 21122 to A.R.B.
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A. J. SucklingM. G. RumsbyM. W. B. Bradbury, Eds.
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To whom correspondence should be addressed at present address: Department of Basic Medical Sciences, Purdue University, School of Veterinary Medicine, Lynn Hall, West Lafayette, IN 47907-1246.