Hyperglycemia and advanced glycation end products disrupt BBB and promote occludin and claudin-5 protein secretion on extracellular microvesicles
Cognitive impairment is a well-known complication of diabetes mellitus (DM). Microvascular compromise was described one DM complication. Recently we showed blood brain barrier (BBB) permeability and memory loss are associated with diminution of tight junctions (TJ) in brain endothelium and pericyte...
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| Veröffentlicht in: | Scientific reports 2020-04, Vol.10 (1), p.7274-7274, Article 7274 |
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| creator | Rom, Slava Heldt, Nathan A. Gajghate, Sachin Seliga, Alecia Reichenbach, Nancy L. Persidsky, Yuri |
| description | Cognitive impairment is a well-known complication of diabetes mellitus (DM). Microvascular compromise was described one DM complication. Recently we showed blood brain barrier (BBB) permeability and memory loss are associated with diminution of tight junctions (TJ) in brain endothelium and pericyte coverage and inflammation in cerebral microvessels and brain tissue paralleling hyperglycemia in mice of both DM types. The current study demonstrates that exposure of brain microvessels to hyperglycemic conditions or advanced glycation end products (AGEs)
ex vivo
resulted in significant abnormalities in membranous distribution of TJ proteins. We found significant increase in the amount of extracellular vesicles (EVs) isolated from DM mice and enhanced presence of TJ proteins, occludin and claudin-5, on EVs. Exposure of BMVECs to high glucose and AGEs led to significant augmentation of ICAM and VCAM expression, elevated leukocyte adhesion to and migration across BMVEC monolayers, and increased BBB permeability
in vitro
. Pericytes exposed to hyperglycemia and AGEs displayed diminished expression of integrin α1, PDGF-R1β and connexin-43. Our findings indicate BBB compromise in DM
ex vivo
,
in vitro
and
in vivo
models in association with BMVEC/pericyte dysfunction and inflammation. Prevention of BBB injury may be a new therapeutic approach to avert cognitive demise in DM. |
| doi_str_mv | 10.1038/s41598-020-64349-x |
| format | Article |
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ex vivo
resulted in significant abnormalities in membranous distribution of TJ proteins. We found significant increase in the amount of extracellular vesicles (EVs) isolated from DM mice and enhanced presence of TJ proteins, occludin and claudin-5, on EVs. Exposure of BMVECs to high glucose and AGEs led to significant augmentation of ICAM and VCAM expression, elevated leukocyte adhesion to and migration across BMVEC monolayers, and increased BBB permeability
in vitro
. Pericytes exposed to hyperglycemia and AGEs displayed diminished expression of integrin α1, PDGF-R1β and connexin-43. Our findings indicate BBB compromise in DM
ex vivo
,
in vitro
and
in vivo
models in association with BMVEC/pericyte dysfunction and inflammation. Prevention of BBB injury may be a new therapeutic approach to avert cognitive demise in DM.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-020-64349-x</identifier><identifier>PMID: 32350344</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/378/1341 ; 692/699/2743/137 ; Advanced glycosylation end products ; Animals ; Blood-brain barrier ; Blood-Brain Barrier - metabolism ; Blood-Brain Barrier - pathology ; Claudin-5 - metabolism ; Cognitive ability ; Connexin 43 ; Diabetes mellitus ; Endothelium ; Extracellular vesicles ; Extracellular Vesicles - metabolism ; Extracellular Vesicles - pathology ; Gene Expression Regulation ; Glycation End Products, Advanced - metabolism ; Glycosylation ; Humanities and Social Sciences ; Hyperglycemia ; Hyperglycemia - metabolism ; Hyperglycemia - pathology ; Leukocyte migration ; Male ; Membrane permeability ; Mice ; Microvasculature ; multidisciplinary ; Occludin - biosynthesis ; Occludin - metabolism ; Pericytes ; Pericytes - metabolism ; Pericytes - pathology ; Permeability ; Platelet-derived growth factor ; Science ; Science (multidisciplinary) ; Tight junctions</subject><ispartof>Scientific reports, 2020-04, Vol.10 (1), p.7274-7274, Article 7274</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c502t-c089a60c59af9758c4b5f11e11e320210a7bbd2f915d4c2f307e6d1d438ddcef3</citedby><cites>FETCH-LOGICAL-c502t-c089a60c59af9758c4b5f11e11e320210a7bbd2f915d4c2f307e6d1d438ddcef3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7190636/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7190636/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,41120,42189,51576,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32350344$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rom, Slava</creatorcontrib><creatorcontrib>Heldt, Nathan A.</creatorcontrib><creatorcontrib>Gajghate, Sachin</creatorcontrib><creatorcontrib>Seliga, Alecia</creatorcontrib><creatorcontrib>Reichenbach, Nancy L.</creatorcontrib><creatorcontrib>Persidsky, Yuri</creatorcontrib><title>Hyperglycemia and advanced glycation end products disrupt BBB and promote occludin and claudin-5 protein secretion on extracellular microvesicles</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Cognitive impairment is a well-known complication of diabetes mellitus (DM). Microvascular compromise was described one DM complication. Recently we showed blood brain barrier (BBB) permeability and memory loss are associated with diminution of tight junctions (TJ) in brain endothelium and pericyte coverage and inflammation in cerebral microvessels and brain tissue paralleling hyperglycemia in mice of both DM types. The current study demonstrates that exposure of brain microvessels to hyperglycemic conditions or advanced glycation end products (AGEs)
ex vivo
resulted in significant abnormalities in membranous distribution of TJ proteins. We found significant increase in the amount of extracellular vesicles (EVs) isolated from DM mice and enhanced presence of TJ proteins, occludin and claudin-5, on EVs. Exposure of BMVECs to high glucose and AGEs led to significant augmentation of ICAM and VCAM expression, elevated leukocyte adhesion to and migration across BMVEC monolayers, and increased BBB permeability
in vitro
. Pericytes exposed to hyperglycemia and AGEs displayed diminished expression of integrin α1, PDGF-R1β and connexin-43. Our findings indicate BBB compromise in DM
ex vivo
,
in vitro
and
in vivo
models in association with BMVEC/pericyte dysfunction and inflammation. Prevention of BBB injury may be a new therapeutic approach to avert cognitive demise in DM.</description><subject>631/378/1341</subject><subject>692/699/2743/137</subject><subject>Advanced glycosylation end products</subject><subject>Animals</subject><subject>Blood-brain barrier</subject><subject>Blood-Brain Barrier - metabolism</subject><subject>Blood-Brain Barrier - pathology</subject><subject>Claudin-5 - metabolism</subject><subject>Cognitive ability</subject><subject>Connexin 43</subject><subject>Diabetes mellitus</subject><subject>Endothelium</subject><subject>Extracellular vesicles</subject><subject>Extracellular Vesicles - metabolism</subject><subject>Extracellular Vesicles - pathology</subject><subject>Gene Expression Regulation</subject><subject>Glycation End Products, Advanced - metabolism</subject><subject>Glycosylation</subject><subject>Humanities and Social Sciences</subject><subject>Hyperglycemia</subject><subject>Hyperglycemia - metabolism</subject><subject>Hyperglycemia - pathology</subject><subject>Leukocyte migration</subject><subject>Male</subject><subject>Membrane permeability</subject><subject>Mice</subject><subject>Microvasculature</subject><subject>multidisciplinary</subject><subject>Occludin - biosynthesis</subject><subject>Occludin - metabolism</subject><subject>Pericytes</subject><subject>Pericytes - metabolism</subject><subject>Pericytes - pathology</subject><subject>Permeability</subject><subject>Platelet-derived growth factor</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Tight junctions</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><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>eNp9Uk1v1DAQtRCIVkv_AAcUiQuXFH8m8QWJraBFqsQFzpbXniyukjjYyWr3Z_CPmeyWUjjUsuTRmzfPM_Yj5DWjl4yK5n2WTOmmpJyWlRRSl_tn5JxTqUouOH_-KD4jFznfUVyKa8n0S3ImuFBUSHlOft0cRkjb7uCgD7awgy-s39nBgS8W1E4hDgUgPKboZzflwoec5nEq1uv1kY-JPk5QROe62YfhCLrOLnGplvQEiGZwCY5qi-B-StZB182dTUUfXIo7yMF1kF-RF63tMlzcnyvy_fOnb1c35e3X6y9XH29LpyifSkcbbSvqlLatrlXj5Ea1jAFuwSln1NabjeetZspLx1tBa6g881I03jtoxYp8OOmO86YHhAZsqTNjCr1NBxNtMP9mhvDDbOPO1EzTSlQo8O5eIMWfM-TJ9CEvM9kB4pwNF7pqlJT4XSvy9j_qXZzTgOMZLmumOPKaJ1moxXEU_LgV4ScWvlnOCdqHlhk1izXMyRoGrWGO1jB7LHrzeNiHkj9GQII4ETKmhi2kv3c_IfsbQqnH8w</recordid><startdate>20200429</startdate><enddate>20200429</enddate><creator>Rom, Slava</creator><creator>Heldt, Nathan A.</creator><creator>Gajghate, Sachin</creator><creator>Seliga, Alecia</creator><creator>Reichenbach, Nancy L.</creator><creator>Persidsky, Yuri</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>88I</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>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20200429</creationdate><title>Hyperglycemia and advanced glycation end products disrupt BBB and promote occludin and claudin-5 protein secretion on extracellular microvesicles</title><author>Rom, Slava ; Heldt, Nathan A. ; Gajghate, Sachin ; Seliga, Alecia ; Reichenbach, Nancy L. ; Persidsky, Yuri</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c502t-c089a60c59af9758c4b5f11e11e320210a7bbd2f915d4c2f307e6d1d438ddcef3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>631/378/1341</topic><topic>692/699/2743/137</topic><topic>Advanced glycosylation end products</topic><topic>Animals</topic><topic>Blood-brain barrier</topic><topic>Blood-Brain Barrier - metabolism</topic><topic>Blood-Brain Barrier - pathology</topic><topic>Claudin-5 - metabolism</topic><topic>Cognitive ability</topic><topic>Connexin 43</topic><topic>Diabetes mellitus</topic><topic>Endothelium</topic><topic>Extracellular vesicles</topic><topic>Extracellular Vesicles - metabolism</topic><topic>Extracellular Vesicles - pathology</topic><topic>Gene Expression Regulation</topic><topic>Glycation End Products, Advanced - metabolism</topic><topic>Glycosylation</topic><topic>Humanities and Social Sciences</topic><topic>Hyperglycemia</topic><topic>Hyperglycemia - metabolism</topic><topic>Hyperglycemia - pathology</topic><topic>Leukocyte migration</topic><topic>Male</topic><topic>Membrane permeability</topic><topic>Mice</topic><topic>Microvasculature</topic><topic>multidisciplinary</topic><topic>Occludin - biosynthesis</topic><topic>Occludin - metabolism</topic><topic>Pericytes</topic><topic>Pericytes - metabolism</topic><topic>Pericytes - pathology</topic><topic>Permeability</topic><topic>Platelet-derived growth factor</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Tight junctions</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rom, Slava</creatorcontrib><creatorcontrib>Heldt, Nathan A.</creatorcontrib><creatorcontrib>Gajghate, Sachin</creatorcontrib><creatorcontrib>Seliga, Alecia</creatorcontrib><creatorcontrib>Reichenbach, Nancy L.</creatorcontrib><creatorcontrib>Persidsky, Yuri</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rom, Slava</au><au>Heldt, Nathan A.</au><au>Gajghate, Sachin</au><au>Seliga, Alecia</au><au>Reichenbach, Nancy L.</au><au>Persidsky, Yuri</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyperglycemia and advanced glycation end products disrupt BBB and promote occludin and claudin-5 protein secretion on extracellular microvesicles</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2020-04-29</date><risdate>2020</risdate><volume>10</volume><issue>1</issue><spage>7274</spage><epage>7274</epage><pages>7274-7274</pages><artnum>7274</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Cognitive impairment is a well-known complication of diabetes mellitus (DM). Microvascular compromise was described one DM complication. Recently we showed blood brain barrier (BBB) permeability and memory loss are associated with diminution of tight junctions (TJ) in brain endothelium and pericyte coverage and inflammation in cerebral microvessels and brain tissue paralleling hyperglycemia in mice of both DM types. The current study demonstrates that exposure of brain microvessels to hyperglycemic conditions or advanced glycation end products (AGEs)
ex vivo
resulted in significant abnormalities in membranous distribution of TJ proteins. We found significant increase in the amount of extracellular vesicles (EVs) isolated from DM mice and enhanced presence of TJ proteins, occludin and claudin-5, on EVs. Exposure of BMVECs to high glucose and AGEs led to significant augmentation of ICAM and VCAM expression, elevated leukocyte adhesion to and migration across BMVEC monolayers, and increased BBB permeability
in vitro
. Pericytes exposed to hyperglycemia and AGEs displayed diminished expression of integrin α1, PDGF-R1β and connexin-43. Our findings indicate BBB compromise in DM
ex vivo
,
in vitro
and
in vivo
models in association with BMVEC/pericyte dysfunction and inflammation. Prevention of BBB injury may be a new therapeutic approach to avert cognitive demise in DM.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32350344</pmid><doi>10.1038/s41598-020-64349-x</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 631/378/1341 692/699/2743/137 Advanced glycosylation end products Animals Blood-brain barrier Blood-Brain Barrier - metabolism Blood-Brain Barrier - pathology Claudin-5 - metabolism Cognitive ability Connexin 43 Diabetes mellitus Endothelium Extracellular vesicles Extracellular Vesicles - metabolism Extracellular Vesicles - pathology Gene Expression Regulation Glycation End Products, Advanced - metabolism Glycosylation Humanities and Social Sciences Hyperglycemia Hyperglycemia - metabolism Hyperglycemia - pathology Leukocyte migration Male Membrane permeability Mice Microvasculature multidisciplinary Occludin - biosynthesis Occludin - metabolism Pericytes Pericytes - metabolism Pericytes - pathology Permeability Platelet-derived growth factor Science Science (multidisciplinary) Tight junctions |
| title | Hyperglycemia and advanced glycation end products disrupt BBB and promote occludin and claudin-5 protein secretion on extracellular microvesicles |
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