Molecular and cellular permeability control at the blood–brain barrier

Gloor, Sergio M.; Wachtel, Marco; Bolliger, Marc; Ishihara, Hideyuki; Landmann, Régine; Frei, Karl

doi:10.1016/s0165-0173(01)00102-3

Cited by 218 publications

(147 citation statements)

References 56 publications

Supporting

Mentioning

145

Contrasting

Unclassified

Order By: Relevance

“…Besides having higher lipophilicity, the blood -brain barrier has specific transport systems and carrier proteins (Gloor et al, 2001). Although He-ALA transport has not yet been studied in neurons or glial cells, in other cell systems ALA and He-ALA seem to be taken up by distinct mechanisms Bermú dez Moretti et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

ALA and ALA hexyl ester induction of porphyrins after their systemic administration to tumour bearing mice

et al. 2002

View full text Add to dashboard Cite

The use of synthetic lipophilic molecules derived from 5-aminolevulinic acid (ALA) is currently under investigation to enhance cellular ALA penetration. In this work we studied the effect of systemic administration to mice of the hexyl ester of ALA (He-ALA) on porphyrin tissue synthesis as compared to ALA. In most normal tissues as well as in tumour, He-ALA induced less porphyrin synthesis than ALA after its systemic administration either intravenous or intraperitoneal, although explant organ cultures exposed to either ALA or He-ALA revealed equally active esterases. The only tissue that accumulated higher porphyrin levels from He-ALA (seven times more than ALA) was the brain, and this correlated well with a rapid increase in ALA/He-ALA content in brain after administration of He-ALA. This may be ascribed to a differential permeability to lipophilic substances controlled by the blood -brain barrier, a feature which could be further exploited to treat brain tumours.

show abstract

Section: Discussionmentioning

confidence: 99%

ALA and ALA hexyl ester induction of porphyrins after their systemic administration to tumour bearing mice

et al. 2002

View full text Add to dashboard Cite

show abstract

“…Within the CNS, the BBB is believed to be formed via glial and cerebral endothelial cell interactions (Janzer and Raff, 1987). Indeed, glial cell processes form end-feet that contact cerebral microvessels, and evidence is building to indicate that glial-derived soluble mediators may induce and maintain the unique cerebral endothelial cell phenotype and hence barrier function (Kniesel and Wolburg, 2000;Gloor et al, 2001). The endothelial BBB phenotype shares many similarities with differentiated intestinal epithelial cells, such as a high transcellular resistance and high levels of ␥-glutamyl transpeptidase activity and glucose transport.…”

Section: Intestinal Mucosa and Blood-brain Barrier Paradigmmentioning

confidence: 99%

Role of enteric glial cells in inflammatory bowel disease

Cabarrocas

Savidge

Liblau

2002

Glia

157

153

View full text Add to dashboard Cite

Enteric glial cells (EGCs) represent an extensive but relatively poorly described cell population within the gastrointestinal tract. Accumulating data suggest that EGCs represent the morphological and functional equivalent of CNS astrocytes within the enteric nervous system (ENS). The EGC network has trophic and protective functions toward enteric neurons and is fully implicated in the integration and the modulation of neuronal activities. Moreover, EGCs seem to be active elements of the ENS during intestinal inflammatory and immune responses, sharing with astrocytes the ability to act as antigen-presenting cells and interacting with the mucosal immune system via the expression of cytokines and cytokine receptors. Transgenic mouse systems have demonstrated that specific ablation of EGC by chemical ablation or autoimmune T-cell targeting induces an intestinal pathology that shows similarities to the early intestinal immunopathology of Crohn's disease. EGCs may also share with astrocytes the ability to regulate tissue integrity, thereby postulating that similar interactions to those observed for the blood-brain barrier may also be partly responsible for regulating mucosal and vascular permeability in the gastrointestinal tract. Disruption of the EGC network in Crohn's disease patients may represent one possible cause for the enhanced mucosal permeability state and vascular dysfunction that are thought to favor mucosal inflammation. GLIA 41:81-93, 2003.

show abstract

“…The BBB is composed of a network of highly specialized endothelial cells surrounded by a basal lamina in both pial and parenchymal vessels. In the latter, however, astrocytic end feet processes ensheath the abluminal surface of these cells playing an important role in the maintenance of vessel impermeability [1,28,62]. The paracellular cleft between adjacent lateral endothelial membranes is almost completely sealed because of the presence of a junctional complex that includes tight junctions (TJs) [44,72,75] and adherens junctions (AJs) [67].…”

Section: Introductionmentioning

confidence: 99%

Evidence for differential changes of junctional complex proteins in murine neurocysticercosis dependent upon CNS vasculature

Alvarez

Teale

2007

Brain Research

View full text Add to dashboard Cite

The delicate balance required to maintain homeostasis of the central nervous system (CNS) is controlled by the blood brain barrier (BBB). Upon injury, the BBB is disrupted compromising the CNS. BBB disruption has been represented as a uniform event. However, our group has shown in a murine model of neurocysticercosis (NCC) that BBB disruption varies depending upon the anatomical site/vascular bed analyzed. In this study further understanding of the mechanisms of BBB disruption were explored in blood vessels located in leptomeninges (pial vessels) and brain parenchyma (parenchymal vessels) by examining the expression of junctional complex proteins in murine brain infected with Mesocestoides corti. Both pial and parenchymal vessels from mock infected animals showed significant colocalization of junctional proteins and displayed an organized architecture. Upon infection, the patterned organization was disrupted and in some cases, particular tight junction and adherens junction proteins were undetectable or appeared to be undergoing proteolysis. The extent and timing of these changes differed between both types of vessels (pial vessel disruption within days versus weeks for parenchymal vessels). To approach potential mechanisms, the expression and activity of matrix metalloproteinase-9 (MMP-9) was evaluated by in situ zymography. The results indicated an increase in MMP-9 activity at sites of BBB disruption exhibiting leukocyte infiltration. Moreover, the timing of MMP activity in pial and parenchymal vessels correlated with the timing of permeability disruption. Thus, breakdown of the BBB is a mutable process despite the similar structure of the junctional complex between pial and parenchymal vessels and involvement of MMP activity.

show abstract

Molecular and cellular permeability control at the blood–brain barrier

Cited by 218 publications

References 56 publications

ALA and ALA hexyl ester induction of porphyrins after their systemic administration to tumour bearing mice

ALA and ALA hexyl ester induction of porphyrins after their systemic administration to tumour bearing mice

Role of enteric glial cells in inflammatory bowel disease

Evidence for differential changes of junctional complex proteins in murine neurocysticercosis dependent upon CNS vasculature

Contact Info

Product

Resources

About