Structure and Pathology of the Blood–Brain Barrier

Nag, S.

doi:10.1007/978-0-387-30380-2_3

Cited by 2 publications

(2 citation statements)

References 287 publications

(276 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Evans blue was later combined with HRP, which has a molecular weight of 40 kDa to facilitate the sampling of areas for ultrastructural studies of BBB breakdown to HRP. The latter studies reported a significant increase in the density of endothelial caveolae only in the vessels with BBB breakdown to HRP within minutes of the onset of pathological states such as acute hypertension, spinal cord injury, seizures, experimental autoimmune encephalomyelitis, excitotoxic brain damage, brain trauma and BBB breakdown induced by bradykinin, histamine and leukotriene C4 [109,122,135]. Transendothelial channels containing HRP were also demonstrated in these studies while passage of HRP via tight junctions was not noted.…”

Section: Tracer Studiesmentioning

confidence: 62%

See 1 more Smart Citation

Review: Molecular pathogenesis of blood–brain barrier breakdown in acute brain injury

Nag

Kapadia

Stewart

2011

Neuropathology Appl Neurobio

Self Cite

140

View full text Add to dashboard Cite

Historically, the blood-brain barrier (BBB) was considered to be at the level of cerebral endothelium. Currently, the interaction of endothelium with other components of the vessel wall and with neurones and glial cells is considered to constitute a functional unit, termed the neurovascular unit that maintains cerebral homeostasis in steady states and brain injury. The emphasis of this review is on cerebral endothelium, the best-studied component of the neurovascular unit, and its permeability mechanisms in health and acute brain injury. Major advances have been made in unravelling the molecular structure of caveolae and tight junctions, both of which are components of the structural barrier to the entry of plasma proteins into brain. Time course studies suggest that caveolar changes precede junctional changes in acute brain injury. Additional factors modulating BBB permeability in acute brain injury are matrix metalloproteinases-2 and 9 and angiogenic factors, the most notable being vascular endothelial growth factor-A and angiopoietins (Ang) 1 and 2. Vascular endothelial growth factor-A and Ang2 have emerged as potent inducers of BBB breakdown while Ang1 is a potent anti-leakage factor. These factors have the potential to modulate permeability in acute brain injury and this is an area of ongoing research. Overall, a combination of haemodynamic, structural and molecular alterations affecting brain endothelium results in BBB breakdown in acute brain injury.

show abstract

Section: Tracer Studiesmentioning

confidence: 62%

“…Occludin, claudins-3, 5 and 12, JAM-A and ZO-1 proteins have been localized in normal cerebral endothelium [58,77,[109][110][111] (Figure 1C,D). Occludin, claudin-5 and JAM-A strands run parallel to the long axis of brain vessels in murine brain [109,111].…”

Section: Tight Junctionsmentioning

confidence: 99%