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• W2743111379 abstract "Abstract The intracellular scaffold KRIT1/CCM1 is an established regulator of vascular barrier function. Loss of KRIT1 leads to decreased microvessel barrier function and to the development of the vascular disorder Cerebral Cavernous Malformation (CCM). However, how loss of KRIT1 causes the subsequent deficit in barrier function remains undefined. Previous studies have shown that loss of KRIT1 increases the production of reactive oxygen species (ROS) and exacerbates vascular permeability triggered by several inflammatory stimuli, but not TNF−α. We now show that endothelial ROS production directly contributes to the loss of barrier function in KRIT1 deficient animals and cells, as targeted antioxidant enzymes reversed the increase in permeability in KRIT1 heterozygous mice as shown by intravital microscopy. Rescue of the redox state restored responsiveness to TNF-α in KRIT1 deficient arterioles, but not venules. In vitro , KRIT1 depletion increased endothelial ROS production via NADPH oxidase signaling, up-regulated Nox4 expression, and promoted NF-κB dependent promoter activity. Recombinant yeast avenanthramide I, an antioxidant and inhibitor of NF-κB signaling, rescued barrier function in KRIT1 deficient cells. However, KRIT1 depletion blunted ROS production in response to TNF-α. Together, our data indicate that ROS signaling is critical for the loss of barrier function following genetic deletion of KRIT1." @default.
• W2743111379 created "2017-08-17" @default.
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• W2743111379 date "2017-08-15" @default.
• W2743111379 modified "2023-09-25" @default.
• W2743111379 title "Up-regulation of NADPH oxidase-mediated redox signaling contributes to the loss of barrier function in KRIT1 deficient endothelium" @default.
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• W2743111379 doi "https://doi.org/10.1038/s41598-017-08373-4" @default.
• W2743111379 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5558000" @default.
• W2743111379 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28811547" @default.
• W2743111379 hasPublicationYear "2017" @default.
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