期刊
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
卷 38, 期 8, 页码 1255-1275出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/0271678X18774666
关键词
Adherens junction; blood-brain barrier; claudin-5; gap junction; intracerebral hemorrhage; intraventricular hemorrhage; occludin; subarachnoid hemorrhage; tight junction; zonula occludens-1
资金
- National Institutes of Health [NS073595, NS079157, NS090925, NS091545, NS093399, NS096917, NS98066, NS098211, AG057928, NIH EY012021]
- Joyce & Don Massey Family Foundation
- Research to Prevent Blindness (RPB)
Vascular disruption is the underlying cause of cerebral hemorrhage, including intracerebral, subarachnoid and intraventricular hemorrhage. The disease etiology also involves cerebral hemorrhage-induced blood-brain barrier (BBB) disruption, which contributes an important component to brain injury after the initial cerebral hemorrhage. BBB loss drives vasogenic edema, allows leukocyte extravasation and may lead to the entry of potentially neurotoxic and vasoactive compounds into brain. This review summarizes current information on changes in brain endothelial junction proteins in response to cerebral hemorrhage (and clot-related factors), the mechanisms underlying junction modification and potential therapeutic targets to limit BBB disruption and, potentially, hemorrhage occurrence. It also addresses advances in the tools that are now available for assessing changes in junctions after cerebral hemorrhage and the potential importance of such junction changes. Recent studies suggest post-translational modification, conformational change and intracellular trafficking of junctional proteins may alter barrier properties. Understanding how cerebral hemorrhage alters BBB properties beyond changes in tight junction protein loss may provide important therapeutic insights to prevent BBB dysfunction and restore normal function.
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