Abstract
The aim of this study was to determine the role of protein kinase C signaling in electromagnetic pulse (EMP)-induced blood-brain barrier (BBB) permeability change in rats. The protein level of total PKC and two PKC isoforms (PKC-alpha, and PKC-beta II) were determined in brain cerebral cortex microvessels by Western blot after exposing rats to EMP at 200kV/m for 200 pulses with 1Hz repetition rate. It was found that the protein level of PKC and PKC-betaII (but not PKC-alpha) in cerebral cortex microvessels increased significantly at 0.5h and 1h after EMP exposure compared with sham-exposed animals and then recovered at 3h. A specific PKC antagonist (H7) almost blocked EMP-induced BBB permeability change. EMP-induced BBB tight junction protein ZO-1 translocation was also inhibited. Our data indicated that PKC signaling was involved in EMP-induced BBB permeability change and ZO-1 translocation in rat.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / pharmacology
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Animals
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Blood-Brain Barrier / drug effects
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Blood-Brain Barrier / enzymology*
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Blood-Brain Barrier / radiation effects
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Cerebral Cortex / metabolism
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Electromagnetic Fields*
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Male
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Membrane Proteins / metabolism
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Microvessels / metabolism
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Permeability / drug effects
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Permeability / radiation effects
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Phosphoproteins / metabolism
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Protein Kinase C / antagonists & inhibitors
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Protein Kinase C / metabolism*
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Protein Kinase C beta
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Protein Kinase Inhibitors / pharmacology
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Protein Transport
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Rats
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Rats, Sprague-Dawley
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Signal Transduction / drug effects
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Signal Transduction / radiation effects
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Zonula Occludens-1 Protein
Substances
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Membrane Proteins
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Phosphoproteins
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Protein Kinase Inhibitors
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Tjp1 protein, rat
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Zonula Occludens-1 Protein
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1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
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Protein Kinase C
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Protein Kinase C beta