Time- and pressure-dependent changes in blood-brain barrier permeability after temporary middle cerebral artery occlusion in rats

1991 ◽  
Vol 82 (4) ◽  
pp. 266-273 ◽  
Author(s):  
D. J. Cole ◽  
J. S. Matsumura ◽  
J. C. Drummond ◽  
R. L. Schultz ◽  
M. H. Wong
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Blood Brain Barrier ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Brain Barrier ◽  
Barrier Permeability ◽  
Blood Brain Barrier Permeability ◽  
Brain Barrier Permeability ◽  
Cerebral Artery Occlusion

The effects of Tanshinone IIA on blood–brain barrier and brain edema after transient middle cerebral artery occlusion in rats

Phytomedicine ◽  
2010 ◽  
Vol 17 (14) ◽  
pp. 1145-1149 ◽  
Author(s):  
Chao Tang ◽  
Hongli Xue ◽  
Changlin Bai ◽  
Rong Fu ◽  
Anhua Wu
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Brain Edema ◽  
Blood Brain Barrier ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Tanshinone Iia ◽  
Brain Barrier ◽  
Blood Brain ◽  
Cerebral Artery Occlusion

scholarly journals Detrimental role of pericyte Nox4 in the acute phase of brain ischemia

2015 ◽  
Vol 36 (6) ◽  
pp. 1143-1154 ◽  
Author(s):  
Ataru Nishimura ◽  
Tetsuro Ago ◽  
Junya Kuroda ◽  
Koichi Arimura ◽  
Masaki Tachibana ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Blood Brain Barrier ◽  
Cerebral Artery ◽  
Infarct Volume ◽  
Artery Occlusion ◽  
Brain Barrier ◽  
Blood Brain ◽  
Barrier Breakdown ◽  
Cerebral Artery Occlusion

Pericytes are mural cells abundantly present in cerebral microvessels and play important roles, including the formation and maintenance of the blood–brain barrier. Nox4 is a major source of reactive oxygen species in cardiovascular cells and modulate cellular functions, particularly under pathological conditions. In the present study, we found that the expression of Nox4 was markedly induced in microvascular cells, including pericytes, in peri-infarct areas after middle cerebral artery occlusion stroke models in mice. The upregulation of Nox4 was greater in a permanent middle cerebral artery occlusion model compared with an ischemia/reperfusion transient middle cerebral artery occlusion model. We performed permanent middle cerebral artery occlusion on mice with Nox4 overexpression in pericytes (Tg-Nox4). Infarct volume was significantly greater with enhanced reactive oxygen species production and blood–brain barrier breakdown in peri-infarct areas in Tg-Nox4, compared with littermate controls. In cultured brain pericytes, Nox4 was significantly upregulated by hypoxia and was promptly downregulated by reoxygenation. Phosphorylation of NFκB and production of matrix metalloproteinase 9 were significantly increased in both cultured pericytes overexpressing Nox4 and in peri-infarct areas in Tg-Nox4. Collectively, Nox4 is upregulated in pericytes in peri-infarct areas after acute brain ischemia and may enhance blood–brain barrier breakdown through activation of NFκB and matrix metalloproteinase 9, thereby causing enlargement of infarct volume.

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