<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lee MJ</submitter><funding>the Bio &amp;amp; Medical Technology Development Program of the National Research Foundation</funding><pagination>475</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8002628</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(3)</volume><pubmed_abstract>Junctional proteins in cerebrovascular endothelial cells are essential for maintaining the barrier function of the blood-brain barrier (BBB), thus protecting the brain from the infiltration of pathogens. The present study showed that the potential therapeutic natural compound auraptene (AUR) enhances junction assembly in cerebrovascular endothelial cells by inducing antioxidant enzymes and the mitochondrial unfolded protein response (mtUPR). Treatment of mouse cerebrovascular endothelial cells with AUR enhanced the expression of junctional proteins, such as occludin, zonula occludens-1 (ZO-1) and vascular endothelial cadherin (VE-cadherin), by increasing the levels of mRNA encoding antioxidant enzymes. AUR treatment also resulted in the depolarization of mitochondrial membrane potential an</pubmed_abstract><journal>Antioxidants (Basel, Switzerland)</journal><pubmed_title>Auraptene Enhances Junction Assembly in Cerebrovascular Endothelial Cells by Promoting Resilience to Mitochondrial Stress through Activation of Antioxidant Enzymes and mtUPR.</pubmed_title><pmcid>PMC8002628</pmcid><funding_grant_id>2019M3E5D1A02068575</funding_grant_id><funding_grant_id>2017R1A5A2015385</funding_grant_id><funding_grant_id>2019R1F1A1059586</funding_grant_id><funding_grant_id>HR20C0025</funding_grant_id><funding_grant_id>the Research Fund of Chungnam National University</funding_grant_id><funding_grant_id>2020R1A6A3A01097081</funding_grant_id><pubmed_authors>Ju X</pubmed_authors><pubmed_authors>Seo C</pubmed_authors><pubmed_authors>Heo JY</pubmed_authors><pubmed_authors>Kim H</pubmed_authors><pubmed_authors>Cui J</pubmed_authors><pubmed_authors>Lee YL</pubmed_authors><pubmed_authors>Go D</pubmed_authors><pubmed_authors>Kang H</pubmed_authors><pubmed_authors>Zhu J</pubmed_authors><pubmed_authors>Jang Y</pubmed_authors><pubmed_authors>Namgung E</pubmed_authors><pubmed_authors>Chung W</pubmed_authors><pubmed_authors>Lee MJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Auraptene Enhances Junction Assembly in Cerebrovascular Endothelial Cells by Promoting Resilience to Mitochondrial Stress through Activation of Antioxidant Enzymes and mtUPR.</name><description>Junctional proteins in cerebrovascular endothelial cells are essential for maintaining the barrier function of the blood-brain barrier (BBB), thus protecting the brain from the infiltration of pathogens. The present study showed that the potential therapeutic natural compound auraptene (AUR) enhances junction assembly in cerebrovascular endothelial cells by inducing antioxidant enzymes and the mitochondrial unfolded protein response (mtUPR). Treatment of mouse cerebrovascular endothelial cells with AUR enhanced the expression of junctional proteins, such as occludin, zonula occludens-1 (ZO-1) and vascular endothelial cadherin (VE-cadherin), by increasing the levels of mRNA encoding antioxidant enzymes. AUR treatment also resulted in the depolarization of mitochondrial membrane potential an</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Mar</publication><modification>2025-04-05T15:23:56.046Z</modification><creation>2022-02-09T14:30:12.693Z</creation></dates><accession>S-EPMC8002628</accession><cross_references><pubmed>33802930</pubmed><doi>10.3390/antiox10030475</doi></cross_references></HashMap>