Inhibition of TNF-α protects in vitro brain barrier from ischaemic damage

Abstract

The version presented here may differ from the published version or from the version of record. If you wish to cite this item you are advised to consult the publisher's version. Please see the repository url above for details on accessing the published version and note that access may require a subscription.For more information, please contact eprints@nottingham.ac.uk activities while improving the barrier function through upregulation of tight junction protein expressions. In conclusion, vitiation of the exaggerated release of TNF-α may be an important therapeutic strategy in preserving cerebral integrity and function during and following a cerebral ischaemic attack.

Anti‐ApoA‐1 IgG serum levels predict worse poststroke outcomes

“…Specifically, we considered age, gender and thrombolysis, previously demonstrated as major determinants of poststroke outcome in large clinical studies [31][32][33]. A direct effect of anti-ApoA-1 IgG on BBB integrity through decreasing astrocyte survival cannot be excluded considering that U251 cells are derived from astrocytes, a key determinant of BBB [37][38][39]. Although preliminary, these results raise several questions that may have a practical clinical implication in the future.…”

“…Even if the exact molecular mechanisms leading to the anti-ApoA-1-IgG-induced apoptosis and necrosis are currently unknown, a role of TLR2, TLR4 and CD14 cannot rule out, considering their expression by glial cells and their involvement in postischaemic brain inflammation [36], Another remaining issue is to know whether and how plasmatic anti-ApoA-1 IgG could migrate through the blood-brain barrier (BBB) into the central nervous system (CNS). A direct effect of anti-ApoA-1 IgG on BBB integrity through decreasing astrocyte survival cannot be excluded considering that U251 cells are derived from astrocytes, a key determinant of BBB [37][38][39]. In this regard, it is very interesting to note that the BBB integrity appears to be a major determinant of the autoantibody's protective, neutral or deleterious effect on brain tissue [3,7].…”

Characterization of cell-cell junction changes associated with the formation of a strong endothelial barrier

“…During inflammation, cytokines alter adherens and tight junctions to allow transmigration of leukocytes and fluid leakage into the CNS. [1][2][3][4][5] Alterations in blood-brain barrier (BBB) permeability are observed in many disease states, including atherosclerosis, diabetes, hypertension, inflammation, sepsis, and HIV. 6,7 Endothelial cells of the BBB are surrounded by other cell types, including astrocytic endfeet, pericytes, microglial and neuronal processes.…”

Imbalance between TNFα and progranulin contributes to memory impairment and anxiety in sleep-deprived mice

“…However, the downstream pathway of PGRN requires further study. TNFα is known to perturb blood-brain barrier integrity and promote brain edema formation51. Thus, it cannot exclude that the increased TNFα may cause the cognitive impairment and anxiety-like behavior by directly destroying the blood-brain barrier integrity.…”