Arsenic-Induced Autophagy in the Developing Mouse Cerebellum: Involvement of the Blood–Brain Barrier’s Tight-Junction Proteins and the PI3K–Akt–mTOR Signaling Pathway

2018 ◽  
Vol 66 (32) ◽  
pp. 8602-8614 ◽  
Author(s):  
Ram Kumar Manthari ◽  
Chiranjeevi Tikka ◽  
Mohammad Mehdi Ommati ◽  
Ruiyan Niu ◽  
Zilong Sun ◽  
...  
Keyword(s):  
Tight Junction ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Tight Junction Proteins ◽  
Mtor Signaling Pathway ◽  
Blood Brain ◽  
Mouse Cerebellum ◽  
Junction Proteins

scholarly journals Interleukin-34 Restores Blood–Brain Barrier Integrity by Upregulating Tight Junction Proteins in Endothelial Cells

PLoS ONE ◽  
2014 ◽  
Vol 9 (12) ◽  
pp. e115981 ◽  
Author(s):  
Shijie Jin ◽  
Yoshifumi Sonobe ◽  
Jun Kawanokuchi ◽  
Hiroshi Horiuchi ◽  
Yi Cheng ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tight Junction ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Tight Junction Proteins ◽  
Barrier Integrity ◽  
Blood Brain ◽  
Blood Brain Barrier Integrity ◽  
Junction Proteins

scholarly journals MicroRNA-30a regulates acute cerebral ischemia-induced blood–brain barrier damage through ZnT4/zinc pathway

2020 ◽  
pp. 0271678X2092678 ◽  
Author(s):  
Peng Wang ◽  
Rong Pan ◽  
John Weaver ◽  
Mengjie Jia ◽  
Xue Yang ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Tight Junction ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Tight Junction Proteins ◽  
Blood Brain ◽  
Acute Cerebral Ischemia ◽  
Junction Proteins

The mechanism of early blood–brain barrier (BBB) disruption after stroke has been intensively studied but still not fully understood. Here, we report that microRNA-30a (miR-30a) could mediate BBB damage using both cellular and animal models of ischemic stroke. In the experiments in vitro, inhibition of miR-30a decreased BBB permeability, prevented the degradation of tight junction proteins, and reduced intracellular free zinc in endothelial cells. We found that the zinc transporter ZnT4 was a direct target of negative regulation by miR-30a, and ZnT4/zinc signaling pathway contributed significantly to miR-30a-mediated BBB damage. Consistent with these in vitro findings, treatment with miR-30a inhibitor reduced zinc accumulation, increased the expression of ZnT4, and prevented the loss of tight junction proteins in microvessels of ischemic animals. Furthermore, inhibition of miR-30a, even at 90 min post onset of middle cerebral artery occlusion, prevented BBB damage, reduced infarct volume, and ameliorated neurological deficits. Together, our findings provide novel insights into the mechanisms of cerebral ischemia-induced BBB disruption and indicate miR-30a as a regulator of BBB function that can be an effective therapeutic target for ischemic stroke.

scholarly journals Differential effects of hydrocortisone and TNFα on tight junction proteins in anin vitromodel of the human blood-brain barrier

2008 ◽  
Vol 586 (7) ◽  
pp. 1937-1949 ◽  
Author(s):  
Carola Förster ◽  
Malgorzata Burek ◽  
Ignacio A. Romero ◽  
Babette Weksler ◽  
Pierre-Olivier Couraud ◽  
...  
Keyword(s):  
Tight Junction ◽  
Blood Brain Barrier ◽  
Human Blood ◽  
Brain Barrier ◽  
Tight Junction Proteins ◽  
Differential Effects ◽  
Blood Brain ◽  
Junction Proteins

Quantitative Atlas of Blood–Brain Barrier Transporters, Receptors, and Tight Junction Proteins in Rats and Common Marmoset

2013 ◽  
Vol 102 (9) ◽  
pp. 3343-3355 ◽  
Author(s):  
Yutaro Hoshi ◽  
Yasuo Uchida ◽  
Masanori Tachikawa ◽  
Takashi Inoue ◽  
Sumio Ohtsuki ◽  
...  
Keyword(s):  
Tight Junction ◽  
Blood Brain Barrier ◽  
Common Marmoset ◽  
Brain Barrier ◽  
Tight Junction Proteins ◽  
Blood Brain ◽  
Junction Proteins
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