scholarly journals Protein Kinase C Activation Modulates Reversible Increase in Cortical Blood–Brain Barrier Permeability and Tight Junction Protein Expression during Hypoxia and Posthypoxic Reoxygenation

2010 ◽  
Vol 30 (11) ◽  
pp. 1847-1859 ◽  
Author(s):  
Colin L Willis ◽  
Diana S Meske ◽  
Thomas P Davis
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Protein Expression ◽  
Tight Junction ◽  
Vascular Permeability ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Kinase C ◽  
Blood Brain ◽  
Junction Protein

Hypoxia (Hx) is a component of many disease states including stroke. Ischemic stroke occurs when there is a restriction of cerebral blood flow and oxygen to part of the brain. During the ischemic, and subsequent reperfusion phase of stroke, blood–brain barrier (BBB) integrity is lost with tight junction (TJ) protein disruption. However, the mechanisms of Hx and reoxygenation (HR)-induced loss of BBB integrity are not fully understood. We examined the role of protein kinase C (PKC) isozymes in modifying TJ protein expression in a rat model of global Hx. The Hx (6% O2) induced increased hippocampal and cortical vascular permeability to 4 and 10 kDa dextran fluorescein isothiocyanate (FITC) and endogenous rat-IgG. Cortical microvessels revealed morphologic changes in nPKC-θ distribution, increased nPKC-θ and aPKC-ζ protein expression, and activation by phosphorylation of nPKC-θ (Thr538) and aPKC-ζ (Thr410) residues after Hx treatment. Claudin-5, occludin, and ZO-1 showed disrupted organization at endothelial cell margins, whereas Western blot analysis showed increased TJ protein expression after Hx. The PKC inhibition with chelerythrine chloride (5 mg/kg intraperitoneally) attenuated Hx-induced hippocampal vascular permeability and claudin-5, PKC (θ and ζ) expression, and phosphorylation. This study supports the hypothesis that nPKC-θ and aPKC-ζ signaling mediates TJ protein disruption resulting in increased BBB permeability.

The role of protein kinase C in the opening of blood–brain barrier induced by electromagnetic pulse

Toxicology ◽  
2010 ◽  
Vol 273 (1-3) ◽  
pp. 29-34 ◽  
Author(s):  
Lian-Bo Qiu ◽  
Gui-Rong Ding ◽  
Kang-Chu Li ◽  
Xiao-Wu Wang ◽  
Yan Zhou ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Blood Brain Barrier ◽  
Electromagnetic Pulse ◽  
Brain Barrier ◽  
Kinase C ◽  
Blood Brain

Protein kinase C restricts transport of carnitine by amino acid transporter ATB0,+ apically localized in the blood–brain barrier

2014 ◽  
Vol 554 ◽  
pp. 28-35 ◽  
Author(s):  
Katarzyna Michalec ◽  
Caroline Mysiorek ◽  
Mélanie Kuntz ◽  
Vincent Bérézowski ◽  
Andrzej A. Szczepankiewicz ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Amino Acid ◽  
Protein Kinase ◽  
Blood Brain Barrier ◽  
Amino Acid Transporter ◽  
Brain Barrier ◽  
Kinase C ◽  
Blood Brain ◽  
Acid Transporter

scholarly journals Protein kinase C-delta inhibition protects blood-brain barrier from sepsis-induced vascular damage

2018 ◽  
Vol 15 (1) ◽  
Author(s):  
Yuan Tang ◽  
Fariborz Soroush ◽  
Shuang Sun ◽  
Elisabetta Liverani ◽  
Jordan C. Langston ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Blood Brain Barrier ◽  
Vascular Damage ◽  
Brain Barrier ◽  
Protein Kinase C Delta ◽  
Kinase C ◽  
Blood Brain

scholarly journals Hydrogen Sulfide Decreases Blood-Brain Barrier Damage via Regulating Protein Kinase C and Tight Junction After Cardiac Arrest in Rats

2018 ◽  
Vol 47 (3) ◽  
pp. 994-1006 ◽  
Author(s):  
Hangbing Li ◽  
Lin Zhu ◽  
Jingwei Feng ◽  
Xiaotong Hu ◽  
Chen Li ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Protein Kinase C ◽  
Hydrogen Sulfide ◽  
Survival Rate ◽  
Protein Kinase ◽  
Blood Brain Barrier ◽  
Evans Blue ◽  
Brain Barrier ◽  
Kinase C ◽  
Blood Brain

Background/Aims: Hydrogen sulfide (H2S) can decrease blood-brain barrier (BBB) permeability after cardiac arrest (CA) and resuscitation; however, the underlying mechanisms are not understood clearly. Methods: We investigated the effects of inhalation of H2S on CA and resuscitation in a rat model of CA. We used Evans blue to detect the integrity of BBB and Western blot to assess the activation of protein kinase c (PKC) isozymes and the expression of Claudin-5, Occludin, and ZO-1. Neurological deficit scales and the 14-days survival rate were measured. Results: We determined that inhalation of 40 p.p.m or 80 p.p.m H2S significantly decreased brain water content and Evans blue leakage, ameliorated neurologic deficit scale and improved 14-days survival rate. H2S inhibited the activation of PKC-α, β I, β II and δ, impelled the activation of PKC-ε, and increased the expression of Claudin-5, Occludin and ZO-1. Conclusions: H2S improved the integrity of BBB, mitigated brain edema; improved neurological outcome and 14-days survival rate in rats after CA and resuscitation. The beneficial effects of H2S may be associated with inhibiting the activation of PKC-α, β I, β II and δ, promoting the activation of PKC-ε, and increasing the expression of Claudin-5, Occludin and ZO-1.

EMP-induced alterations of tight junction protein expression and disruption of the blood–brain barrier

2010 ◽  
Vol 196 (3) ◽  
pp. 154-160 ◽  
Author(s):  
Gui-Rong Ding ◽  
Lian-Bo Qiu ◽  
Xiao-Wu Wang ◽  
Kang-Chu Li ◽  
Yong-Chun Zhou ◽  
...  
Keyword(s):  
Protein Expression ◽  
Tight Junction ◽  
Blood Brain Barrier ◽  
Tight Junction Protein ◽  
Brain Barrier ◽  
Tight Junction Protein Expression ◽  
Blood Brain ◽  
Junction Protein
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