Cell surface endothelial proteins altered in experimental allergic encephalomyelitis

Sternberger, Nancy H.; Sternberger, Ludwig A.; Kies, Marian W.; Shear, Charles R.

doi:10.1016/0165-5728(89)90180-x

Cited by 67 publications

(36 citation statements)

References 24 publications

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“…pressed where the BBB is healthy and fully developed (Sternberger et al, 1989;Cassella et al, 1996). Weak or absent EBA staining is considered as a marker of BBB disruption (Sternberger et al, 1989;Nishigaya et al, 2000;Zhu et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

“…Weak or absent EBA staining is considered as a marker of BBB disruption (Sternberger et al, 1989;Nishigaya et al, 2000;Zhu et al, 2001). Studies addressing the time course of EBA expression after brain injury have shown that its downregulation precedes neovessel formation and that reexpression of the EBA antigen occurs within a narrow time window (Rosenstein et al, 1992;Nishigaya et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…EBA is only expressed in blood vessels with fully developed BBB properties (Sternberger et al, 1989;Cassella et al, 1996). In control animals, EBA-positive vessels were evenly distributed in all parts of the brain but for the areas without a functional BBB (e.g., median eminence and area postrema).…”

Section: The Bbb Is Defective In Dyskinetic Animalsmentioning

confidence: 99%

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Endothelial Proliferation and Increased Blood–Brain Barrier Permeability in the Basal Ganglia in a Rat Model of 3,4-Dihydroxyphenyl-l-Alanine-Induced Dyskinesia

Westin

Lindgren²,

Gardi³

et al. 2006

J. Neurosci.

117

132

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3,4-Dihydroxyphenyl-L-alanine (L-DOPA)-induced dyskinesia is associated with molecular and synaptic plasticity in the basal ganglia, but the occurrence of structural remodeling through cell genesis has not been explored. In this study, rats with 6-hydroxydopamine lesions received injections of the thymidine analog 5-bromo-2Ј-deoxyuridine (BrdU) concomitantly with L-DOPA for 2 weeks. A large number of BrdU-positive cells were found in the striatum and its output structures (globus pallidus, entopeduncular nucleus, and substantia nigra pars reticulata) in L-DOPA-treated rats that had developed dyskinesia. The vast majority (60 -80%) of the newborn cells stained positively for endothelial markers. This endothelial proliferation was associated with an upregulation of immature endothelial markers (nestin) and a downregulation of endothelial barrier antigen on blood vessel walls. In addition, dyskinetic rats exhibited a significant increase in total blood vessel length and a visible extravasation of serum albumin in the two structures in which endothelial proliferation was most pronounced (substantia nigra pars reticulata and entopeduncular nucleus). The present study provides the first evidence of angiogenesis and blood-brain barrier dysfunction in an experimental model of L-DOPA-induced dyskinesia. These microvascular changes are likely to affect the kinetics of L-DOPA entry into the brain, favoring the occurrence of motor complications.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Endothelial Proliferation and Increased Blood–Brain Barrier Permeability in the Basal Ganglia in a Rat Model of 3,4-Dihydroxyphenyl-l-Alanine-Induced Dyskinesia

Westin

Lindgren²,

Gardi³

et al. 2006

J. Neurosci.

117

132

View full text Add to dashboard Cite

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“…EBA is a protein triplet of molecular weights 32, 25 and 23.5 kDa located in the plasma membrane of brain endothelial microvessels (Sternberger et al, 1989). EBA immunoreactivity decreases to nadir at 3 days after focal ischemia and then increases but not to the level of contralateral side even until 28 days after ischemia (Lin and Ginsberg, 2000).…”

Section: Discussionmentioning

confidence: 99%

Combined treatment of vascular endothelial growth factor and human neural stem cells in experimental focal cerebral ischemia

Chu

Park

Lee

et al. 2005

Neuroscience Research

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“…The mechanisms by which the BBB permeability increases during the disease process in EAE are not completely understood; however, it is thought that it involves a combination of cell mediated injury, and molecular dependent disorganisation of BBB structures, e.g. loss of the tight junction proteins occludin and zonula occludens-1 (Bolton et al, 1998), loss of endothelial barrier antigens (Sternberger et al, 1989), and proteolytic degradation of the extracellular matrix.…”

Section: Introductionmentioning

confidence: 99%

Blood–brain barrier disruption and lesion localisation in experimental autoimmune encephalomyelitis with predominant cerebellar and brainstem involvement

Muller

Pender

Greer

2005

Journal of Neuroimmunology

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The role of the blood-brain barrier (BBB) in determining lesion distribution was assessed in an atypical model of experimental autoimmune encephalomyelitis (EAE) induced in C3H/HeJ mice by immunisation with peptide 190-209 of myelin proteolipid protein, which can result in two distinct types of EAE, each with distinct lesion distribution. Areas of the BBB showing constitutively greater permeability in naïve mice did not correlate with the lesion distribution in EAE. BBB disruption occurred only in sites of inflammatory cell infiltration. Irrespective of the clinical type, the BBB was disrupted in the cerebellum and brainstem. Pertussis toxin had no effect on lesion distribution. Thus, lesion distribution is not influenced solely by BBB permeability.

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Cell surface endothelial proteins altered in experimental allergic encephalomyelitis

Cited by 67 publications

References 24 publications

Endothelial Proliferation and Increased Blood–Brain Barrier Permeability in the Basal Ganglia in a Rat Model of 3,4-Dihydroxyphenyl-l-Alanine-Induced Dyskinesia

Endothelial Proliferation and Increased Blood–Brain Barrier Permeability in the Basal Ganglia in a Rat Model of 3,4-Dihydroxyphenyl-l-Alanine-Induced Dyskinesia

Combined treatment of vascular endothelial growth factor and human neural stem cells in experimental focal cerebral ischemia

Blood–brain barrier disruption and lesion localisation in experimental autoimmune encephalomyelitis with predominant cerebellar and brainstem involvement

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