Hepatocyte growth factor attenuates cerebral ischemia-induced increase in permeability of the blood–brain barrier and decreases in expression of tight junctional proteins in cerebral vessels

2006 ◽  
Vol 407 (2) ◽  
pp. 141-145 ◽  
Author(s):  
Ichiro Date ◽  
Norio Takagi ◽  
Keiko Takagi ◽  
Kouichi Tanonaka ◽  
Hiroshi Funakoshi ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Blood Brain Barrier ◽  
Cerebral Vessels ◽  
Brain Barrier ◽  
Junctional Proteins ◽  
Blood Brain ◽  
Hepatocyte Growth

Permeation of hepatocyte growth factor across the blood–brain barrier

2006 ◽  
Vol 201 (1) ◽  
pp. 99-104 ◽  
Author(s):  
Weihong Pan ◽  
Yongmei Yu ◽  
Ruth Yemane ◽  
Courtney Cain ◽  
Chuanhui Yu ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Blood Brain ◽  
Hepatocyte Growth

scholarly journals PDGFR-β restores blood-brain barrier functions in a mouse model of focal cerebral ischemia

2018 ◽  
Vol 39 (8) ◽  
pp. 1501-1515 ◽  
Author(s):  
Jie Shen ◽  
Guihua Xu ◽  
Runxiu Zhu ◽  
Jun Yuan ◽  
Yoko Ishii ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Growth Factor ◽  
Blood Brain Barrier ◽  
Transforming Growth Factor ◽  
Focal Cerebral Ischemia ◽  
Brain Barrier ◽  
Ischemic Lesion ◽  
Blood Brain ◽  
Tgf Β1

Although platelet-derived growth factor receptor beta (PDGFR-β) mediates the recruitment of vascular pericytes into ischemic lesion to restore the blood-brain barrier (BBB) dysfunction, its mechanisms still remain elusive . Compared with control PDGFR-βfloxed/floxed mice (Floxed), postnatally induced systemic PDGFR-β knockout mice (Esr-KO) not only showed severe brain edema, neurologic functional deficits, decreased expression of tight junction (TJ) proteins, abundant endothelial transcytosis, and deformed TJs in the BBB, but also showed reduced expression of transforming growth factor-β (TGF-β) protein after photothrombotic middle cerebral artery occlusion (MCAO). In endothelial-pericyte co-culture, an in vitro model of BBB, the increment in the barrier function of endothelial monolayer induced by pericyte co-culture was completely cancelled by silencing PDGFR-β gene expression in pericytes, and was additively improved by PDGFR-β and TGF-β receptor signals under hypoxia condition. Exogenous PDGF-BB increased the expression of p-Smad2/3, while anti-TGF-β1 antibody at least partially inhibited the phosphorylation of Smad2/3 after PDGF-BB treatment in vitro. Furthermore, pre-administration of TGF-β1 partially alleviated edema formation, neurologic dysfunction, and TJs reduction in Esr-KO mice after MCAO. Accordingly, PDGFR-β signalling, via TGF-β signalling, may be crucial for restoration of BBB integrity after cerebral ischemia and therefore represents a novel potential therapeutic target.

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