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Open AccessJournal ArticleDOI

Glial influence on the blood brain barrier.

Jorge I. Alvarez, +2 more
- 01 Dec 2013 - 
- Vol. 61, Iss: 12, pp 1939-1958
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TLDR
Recent findings related to the involvement of astrocytes and endothelial cells, including radial glial cells, in the induction of barrier properties during embryogenesis and adulthood are described.
Abstract
The Blood Brain Barrier (BBB) is a specialized vascular structure tightly regulating central nervous system (CNS) homeostasis. Endothelial cells are the central component of the BBB and control of their barrier phenotype resides on astrocytes and pericytes. Interactions between these cells and the endothelium promote and maintain many of the physiological and metabolic characteristics that are unique to the BBB. In this review we describe recent findings related to the involvement of astroglial cells, including radial glial cells, in the induction of barrier properties during embryogenesis and adulthood. In addition, we describe changes that occur in astrocytes and endothelial cells during injury and inflammation with a particular emphasis on alterations of the BBB phenotype.

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Citations
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The Blood–Brain Barrier

TL;DR: Understanding how these different cell populations interact to regulate the barrier properties is essential for understanding how the brain functions during health and disease.
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The blood–brain barrier and blood–tumour barrier in brain tumours and metastases

TL;DR: A deeper understanding of the BBB and BTB through the application of single-cell sequencing and imaging techniques, and the development of biomarkers of BBB integrity along with systems biology approaches, should enable new personalized treatment strategies for primary brain malignancies and brain metastases.
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Astrocyte Reactivity and Reactive Astrogliosis: Costs and Benefits

TL;DR: Understanding the multifaceted roles of astrocytes in the healthy and diseased CNS will undoubtedly contribute to the development of treatment strategies that will, in a context-dependent manner and at appropriate time points, modulate reactive astrogliosis to promote brain repair and reduce the neurological impairment.
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Overcoming the blood-brain tumor barrier for effective glioblastoma treatment

TL;DR: Methods to overcome the blood-brain tumor barrier barrier (BBTB) are provided, including osmotic blood- brain barrier disruption (BBBD), bradykinin receptor-mediated BBTB opening, inhibition of multidrug efflux transporters, receptor- mediated transport systems and physiological circumvention of the BBTB.
References
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Journal ArticleDOI

Endothelial adherens junctions control tight junctions by VE-cadherin-mediated upregulation of claudin-5.

TL;DR: It is shown that endothelial VE-cadherin at AJs upregulates the gene encoding the TJ adhesive protein claudin-5, and this effect requires the release of the inhibitory activity of forkhead box factor FoxO1 and the Tcf-4–β-catenin transcriptional repressor complex.
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The large apparent work capability of the blood‐brain barrier: A study of the mitochondrial content of capillary endothelial cells in brain and other tissues of the rat

TL;DR: The apparent excess metabolic work capability of the BBB suggested by this greater number of mitochondria may be related to maintenance of ion differentials between blood plasma and brain extracellular fluid, to extrachoroidal cerebrospinal fluid formation, or to maintaining the unique structural characteristics of central nervous system capillaries.
Journal ArticleDOI

Minireview: Overview of the Renin-Angiotensin System—An Endocrine and Paracrine System

TL;DR: Recent advances in understanding the relationship between endocrine and paracrine (tissue) RAS using transgenic models are discussed in a minireview of renin-angiotensin system.
Journal ArticleDOI

VEGF-mediated disruption of endothelial CLN-5 promotes blood-brain barrier breakdown.

TL;DR: The endothelial transmembrane tight junction proteins claudin-5 (CLN-5) and occludin (OCLN) are identified as targets of VEGF-A action and down-regulation by VEGf-A constitutes a significant mechanism in BBB breakdown.
Journal ArticleDOI

Regulation of tight junctions and loss of barrier function in pathophysiology

TL;DR: Potential mechanisms by which elevated growth factors elicit deregulated paracellular permeability via altered regulation of tight junctions are elucidated, with particular emphasis on the tight junction proteins occludin and ZO-1, protein kinase C signaling, and endocytosis of junctional proteins.
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Trending Questions (1)
What is the brain, BBB and microglia?

The paper does not provide information about the brain or microglia. The paper is about the influence of glial cells on the blood brain barrier (BBB).