Glucocorticoids increase VE-cadherin expression and cause cytoskeletal rearrangements in murine brain endothelial cEND cells
Recent studies have shown the influence of glucocorticoids on the expression of the tight junction protein occludin in the brain capillary endothelial cell line cEND, contributing to improvement in endothelial barrier functions. In this study, we investigated glucocorticoid effects on the expression...
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| Veröffentlicht in: | Journal of cerebral blood flow and metabolism 2008-06, Vol.28 (6), p.1139-1149 |
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| creator | Blecharz, Kinga G Drenckhahn, Detlev Förster, Carola Y |
| description | Recent studies have shown the influence of glucocorticoids on the expression of the tight junction protein occludin in the brain capillary endothelial cell line cEND, contributing to improvement in endothelial barrier functions. In this study, we investigated glucocorticoid effects on the expression of the adherens junction proteins VE- (vascular-endothelial) cadherin, α-catenin and β-catenin as well as that of ZO-1, the plaque protein shared by both adherens and tight junctions on stimulation with dexamethasone. We were able to show a positive influence of dexamethasone administration on VE-cadherin protein levels as well as a rearrangement of VE-cadherin protein to the cytoskeleton after dexamethasone treatment. Investigation of transcriptional activation of the VE-cadherin promoter by dexamethasone, however, did not point to direct glucocorticoid-mediated VE-cadherin gene induction but rather suggested indirect steroid effects leading to increased VE-cadherin protein synthesis. Dexamethasone was further shown to induce cellular differentiation into a cobblestone cellular morphology and reinforcement of adherens junctions concomitant with the increased anchorage of VE-cadherin to the actin cytoskeleton. We thus propose that glucocorticoid effects on VE-cadherin protein synthesis and organization are important for the formation of both adherens and tight junction, and for improved barrier properties in microvascular brain endothelial cells. |
| doi_str_mv | 10.1038/jcbfm.2008.2 |
| format | Article |
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In this study, we investigated glucocorticoid effects on the expression of the adherens junction proteins VE- (vascular-endothelial) cadherin, α-catenin and β-catenin as well as that of ZO-1, the plaque protein shared by both adherens and tight junctions on stimulation with dexamethasone. We were able to show a positive influence of dexamethasone administration on VE-cadherin protein levels as well as a rearrangement of VE-cadherin protein to the cytoskeleton after dexamethasone treatment. Investigation of transcriptional activation of the VE-cadherin promoter by dexamethasone, however, did not point to direct glucocorticoid-mediated VE-cadherin gene induction but rather suggested indirect steroid effects leading to increased VE-cadherin protein synthesis. Dexamethasone was further shown to induce cellular differentiation into a cobblestone cellular morphology and reinforcement of adherens junctions concomitant with the increased anchorage of VE-cadherin to the actin cytoskeleton. We thus propose that glucocorticoid effects on VE-cadherin protein synthesis and organization are important for the formation of both adherens and tight junction, and for improved barrier properties in microvascular brain endothelial cells.</description><identifier>ISSN: 0271-678X</identifier><identifier>EISSN: 1559-7016</identifier><identifier>DOI: 10.1038/jcbfm.2008.2</identifier><identifier>PMID: 18231113</identifier><identifier>CODEN: JCBMDN</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Actins - metabolism ; Animals ; Antigens, CD - metabolism ; Biological and medical sciences ; Brain - cytology ; Cadherins - metabolism ; Cell Line ; Cell Shape - drug effects ; Cytoskeleton - drug effects ; Cytoskeleton - metabolism ; Dexamethasone - pharmacology ; Endothelial Cells - cytology ; Gene Expression Regulation - drug effects ; Glucocorticoids - pharmacology ; Humans ; Investigative techniques, diagnostic techniques (general aspects) ; Medical sciences ; Mice ; Nervous system ; Neurology ; Promoter Regions, Genetic - genetics ; Transcription, Genetic - genetics ; Transcriptional Activation - drug effects ; Ultrasonic investigative techniques ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Journal of cerebral blood flow and metabolism, 2008-06, Vol.28 (6), p.1139-1149</ispartof><rights>2008 ISCBFM</rights><rights>2008 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jun 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c541t-bcd258b1a42680dc1b16daff09827c7133817374b8db2866a06fe529aa65614e3</citedby><cites>FETCH-LOGICAL-c541t-bcd258b1a42680dc1b16daff09827c7133817374b8db2866a06fe529aa65614e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1038/jcbfm.2008.2$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1038/jcbfm.2008.2$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,778,782,21802,27907,27908,43604,43605</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20411973$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18231113$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Blecharz, Kinga G</creatorcontrib><creatorcontrib>Drenckhahn, Detlev</creatorcontrib><creatorcontrib>Förster, Carola Y</creatorcontrib><title>Glucocorticoids increase VE-cadherin expression and cause cytoskeletal rearrangements in murine brain endothelial cEND cells</title><title>Journal of cerebral blood flow and metabolism</title><addtitle>J Cereb Blood Flow Metab</addtitle><description>Recent studies have shown the influence of glucocorticoids on the expression of the tight junction protein occludin in the brain capillary endothelial cell line cEND, contributing to improvement in endothelial barrier functions. In this study, we investigated glucocorticoid effects on the expression of the adherens junction proteins VE- (vascular-endothelial) cadherin, α-catenin and β-catenin as well as that of ZO-1, the plaque protein shared by both adherens and tight junctions on stimulation with dexamethasone. We were able to show a positive influence of dexamethasone administration on VE-cadherin protein levels as well as a rearrangement of VE-cadherin protein to the cytoskeleton after dexamethasone treatment. Investigation of transcriptional activation of the VE-cadherin promoter by dexamethasone, however, did not point to direct glucocorticoid-mediated VE-cadherin gene induction but rather suggested indirect steroid effects leading to increased VE-cadherin protein synthesis. Dexamethasone was further shown to induce cellular differentiation into a cobblestone cellular morphology and reinforcement of adherens junctions concomitant with the increased anchorage of VE-cadherin to the actin cytoskeleton. We thus propose that glucocorticoid effects on VE-cadherin protein synthesis and organization are important for the formation of both adherens and tight junction, and for improved barrier properties in microvascular brain endothelial cells.</description><subject>Actins - metabolism</subject><subject>Animals</subject><subject>Antigens, CD - metabolism</subject><subject>Biological and medical sciences</subject><subject>Brain - cytology</subject><subject>Cadherins - metabolism</subject><subject>Cell Line</subject><subject>Cell Shape - drug effects</subject><subject>Cytoskeleton - drug effects</subject><subject>Cytoskeleton - metabolism</subject><subject>Dexamethasone - pharmacology</subject><subject>Endothelial Cells - cytology</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Glucocorticoids - pharmacology</subject><subject>Humans</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Nervous system</subject><subject>Neurology</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Transcription, Genetic - genetics</subject><subject>Transcriptional Activation - drug effects</subject><subject>Ultrasonic investigative techniques</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0271-678X</issn><issn>1559-7016</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp90c9rFDEUB_Agit1Wb54lCCqCs-Ylkx9zlHatQtGLirchk3nTzjqTbJMZsOAfb6a7tCDoKZdPvnkvX0KeAVsDE-bd1jXduOaMmTV_QFYgZVVoBuohWTGuoVDa_DgixyltWTZCysfkCAwXACBW5Pf5MLvgQpx6F_o20d67iDYh_b4pnG2vMPae4q9dxJT64Kn1LXV2zsDdTCH9xAEnO9B8J0brL3FEPy0pdJzzTaRNtEuAb8N0hUOfqdt8PqMOhyE9IY86OyR8ejhPyLcPm6-nH4uLL-efTt9fFE6WMBWNa7k0DdiSK8NaBw2o1nYdqwzXToMQBrTQZWPahhulLFMdSl5Zq6SCEsUJeb3P3cVwPWOa6rFPywTWY5hTbbTiJYBkWb76r9RMl1pznuGLv-A2zNHnLWoOVSkkKJXR2z1yMaQUsat3sR9tvKmB1Ut59W159VJevWQ-P2TOzYjtPT60lcHLA7DJ2aHLH-76dOc4y0tUenFv9i7ZS7wf7B-P0r31dpoj3oXdosVw8QcijLxH</recordid><startdate>20080601</startdate><enddate>20080601</enddate><creator>Blecharz, Kinga G</creator><creator>Drenckhahn, Detlev</creator><creator>Förster, Carola Y</creator><general>SAGE Publications</general><general>Lippincott Williams & Wilkins</general><general>Sage Publications Ltd</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7TK</scope></search><sort><creationdate>20080601</creationdate><title>Glucocorticoids increase VE-cadherin expression and cause cytoskeletal rearrangements in murine brain endothelial cEND cells</title><author>Blecharz, Kinga G ; 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In this study, we investigated glucocorticoid effects on the expression of the adherens junction proteins VE- (vascular-endothelial) cadherin, α-catenin and β-catenin as well as that of ZO-1, the plaque protein shared by both adherens and tight junctions on stimulation with dexamethasone. We were able to show a positive influence of dexamethasone administration on VE-cadherin protein levels as well as a rearrangement of VE-cadherin protein to the cytoskeleton after dexamethasone treatment. Investigation of transcriptional activation of the VE-cadherin promoter by dexamethasone, however, did not point to direct glucocorticoid-mediated VE-cadherin gene induction but rather suggested indirect steroid effects leading to increased VE-cadherin protein synthesis. Dexamethasone was further shown to induce cellular differentiation into a cobblestone cellular morphology and reinforcement of adherens junctions concomitant with the increased anchorage of VE-cadherin to the actin cytoskeleton. 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| ispartof | Journal of cerebral blood flow and metabolism, 2008-06, Vol.28 (6), p.1139-1149 |
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| subjects | Actins - metabolism Animals Antigens, CD - metabolism Biological and medical sciences Brain - cytology Cadherins - metabolism Cell Line Cell Shape - drug effects Cytoskeleton - drug effects Cytoskeleton - metabolism Dexamethasone - pharmacology Endothelial Cells - cytology Gene Expression Regulation - drug effects Glucocorticoids - pharmacology Humans Investigative techniques, diagnostic techniques (general aspects) Medical sciences Mice Nervous system Neurology Promoter Regions, Genetic - genetics Transcription, Genetic - genetics Transcriptional Activation - drug effects Ultrasonic investigative techniques Vascular diseases and vascular malformations of the nervous system |
| title | Glucocorticoids increase VE-cadherin expression and cause cytoskeletal rearrangements in murine brain endothelial cEND cells |
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