The blood–brain barrier in trauma, stroke and edema

Verlooy, Jan; Reempts, Jos Van

doi:10.1016/j.ics.2005.02.025

Cited by 3 publications

(3 citation statements)

References 10 publications

(10 reference statements)

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“…Interestingly, in a model of traumatic spinal cord injury in the same Tg mouse line, we also observed increased vascular permeability in HuR Tg mice compared to Wt littermates [22]. When the two studies are considered together, ectopic HuR appears to modulate common downstream pathways in two remarkably different CNS injury models [36]. …”

Section: Discussionmentioning

confidence: 99%

Transgenic expression of HuR increases vasogenic edema and impedes functional recovery in rodent ischemic stroke

Ardelt

Carpenter

Iwuchukwu

et al. 2017

Neuroscience Letters

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Background and Purpose Ischemic stroke produces significant morbidity and mortality, and acute interventions are limited by short therapeutic windows. Novel approaches to neuroprotection and neurorepair are necessary. HuR is an RNA binding protein (RBP) which modulates RNA stability and translational efficiency of genes linked to ischemic stroke injury. Methods Using a transgenic (Tg) mouse model, we examined the impact of ectopic HuR expression in astrocytes on acute injury evolution after transient middle cerebral artery occlusion (tMCAO). Results HuR transgene expression was detected in astrocytes in perilesional regions and contralaterally. HuR Tg mice did not improve neurologically 72 hours after injury, whereas littermate controls did. In Tg mice, increased cerebral vascular permeability and edema were observed. Infarct volume was not affected by the presence of the transgene. Conclusions Ectopic expression of HuR in astrocytes worsens outcome after transient ischemic stroke in mice in part by increasing vasogenic cerebral edema. These findings suggest that HuR could be a therapeutic target in cerebral ischemia/reperfusion.

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Section: Discussionmentioning

confidence: 99%

Transgenic expression of HuR increases vasogenic edema and impedes functional recovery in rodent ischemic stroke

Ardelt

Carpenter

Iwuchukwu

et al. 2017

Neuroscience Letters

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“…Scientific discussion of this is infrequent in the clinical neurological literature perhaps because of its rapidly evolving and sometimes contradictory scientific underpinning. For example, agreement has only recently been reached on the existence and roles of molecules present in ‘typical’ epithelial and endothelial tight junctions’[45,52] and in the human CNS barrier endothelium [2,4,8,13]. It has taken some time, for example, to establish the importance of the claudin family (of which there are at least 20 members) in determining the establishment of tight junctional strands and the extent and specificity of paracellular permeability in different tissues and organs [52].…”

Section: Discussionmentioning

confidence: 99%

“…Adverse and often rapid impairment of the blood-brain barrier occurs in a variety of human diseases, including, but not restricted to, those with autoimmune, infective, toxic, traumatic, neoplastic and ischemic/hypoxic pathol-ogies [1][2][3][4][5][6]. Whatever the initial mechanism of barrier damage in these disorders, the establishment of an associated inflammatory reaction adds to the risk that initial barrier damage and leak may extend or persist [2,4,7,8]. Despite insights from experimental in vivo and in vitro models [2,7,[9][10][11][12][13][14], progress in revealing the full extent, duration and mechanisms of barrier dysfunction in human neuroinflammation has been slow.…”

Section: Introductionmentioning

confidence: 99%

Persistent endothelial abnormalities and blood–brain barrier leak in primary and secondary progressive multiple sclerosis

Leech

Kirk

Plumb

et al. 2007

Neuropathology Appl Neurobio

114

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Epithelial and endothelial tight junctions are pathologically altered in infectious, inflammatory, neoplastic and other diseases. Previously, we described such abnormalities, associated with serum protein leak, in tight junctions of the blood–brain barrier endothelium, in lesional and normal‐appearing white matter (NAWM) in secondary progressive (SP) and acute multiple sclerosis (MS). This work is extended here to lesions and NAWM in primary progressive multiple sclerosis (PPMS) and to cortical grey matter in PPMS and SPMS. Immunocytochemistry and semiquantitative confocal microscopy for the tight junction protein zonula occludens 1 (ZO‐1) was performed on snap‐frozen sections from PPMS (n = 6) and controls (n = 5). Data on 2103 blood vessels were acquired from active lesions (n = 10), inactive lesions (n = 15), NAWM (n = 42) and controls (n = 20). Data on 1218 vessels were acquired from normal‐appearing grey matter (PPMS, 5; SPMS, 6; controls, 5). In PPMS abnormal ZO‐1 expression in active white matter lesions and NAWM, was found in 42% and 13% of blood vessels, respectively, comparable to previous data from acute and SPMS. In chronic white matter plaques, however, abnormalities were considerably more frequent (37%) in PPMS than in SPMS. Abnormality was also more frequent in normal‐appearing grey matter in SPMS (23%) than in PPMS (10%). In summary, abnormal tight junctions in both SPMS and PPMS are most frequent in active white matter lesions but persist in inactive lesions, particularly in PPMS. Abnormal tight junctions are also common in normal‐appearing grey matter in SPMS. Persistent endothelial abnormality with leak (PEAL) is therefore widespread but variably expressed in MS and may contribute to disease progression.

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PhoTOChemically Based Models of Focal Experimental Thrombotic Stroke in Rodents

Watson¹,

Prado²

2008

Manual of Stroke Models in Rats

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The blood–brain barrier in trauma, stroke and edema

Cited by 3 publications

References 10 publications

Transgenic expression of HuR increases vasogenic edema and impedes functional recovery in rodent ischemic stroke

Transgenic expression of HuR increases vasogenic edema and impedes functional recovery in rodent ischemic stroke

Persistent endothelial abnormalities and blood–brain barrier leak in primary and secondary progressive multiple sclerosis

PhoTOChemically Based Models of Focal Experimental Thrombotic Stroke in Rodents

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