Tight junctions in brain barriers during central nervous system inflammation

Coisne, Caroline; Engelhardt, Britta (2011). Tight junctions in brain barriers during central nervous system inflammation. Antioxidants & redox signalling, 15(5), pp. 1285-303. Larchmont, N.Y.: Mary Ann Liebert 10.1089/ars.2011.3929

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Homeostasis within the central nervous system (CNS) is a prerequisite to elicit proper neuronal function. The CNS is tightly sealed from the changeable milieu of the blood stream by the blood-brain barrier (BBB) and the blood-cerebrospinal fluid (CSF) barrier (BCSFB). Whereas the BBB is established by specialized endothelial cells of CNS microvessels, the BCSFB is formed by the epithelial cells of the choroid plexus. Both constitute physical barriers by a complex network of tight junctions (TJs) between adjacent cells. During many CNS inflammatory disorders, such as multiple sclerosis, human immunodeficiency virus infection, or Alzheimer's disease, production of pro-inflammatory cytokines, matrix metalloproteases, and reactive oxygen species are responsible for alterations of CNS barriers. Barrier dysfunction can contribute to neurological disorders in a passive way by vascular leakage of blood-borne molecules into the CNS and in an active way by guiding the migration of inflammatory cells into the CNS. Both ways may directly be linked to alterations in molecular composition, function, and dynamics of the TJ proteins. This review summarizes current knowledge on the cellular and molecular aspects of the functional and dysfunctional TJ complexes at the BBB and the BCSFB, with a particular emphasis on CNS inflammation and the role of reactive oxygen species.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > Theodor Kocher Institute

UniBE Contributor:

Coisne, Caroline Marie and Engelhardt, Britta

ISSN:

1523-0864

Publisher:

Mary Ann Liebert

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 14:23

Last Modified:

06 Dec 2013 13:28

Publisher DOI:

10.1089/ars.2011.3929

PubMed ID:

21338320

Web of Science ID:

000293576300009

URI:

https://boris.unibe.ch/id/eprint/7795 (FactScience: 213131)

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