Brain endothelial hemostasis regulation by pericytes
Pericytes are known to regulate brain capillary endothelial functions. The purpose of this study was to define the hemostatic regulatory role of human brain pericytes. We used blood–brain barrier models consisting of human pericytes grown on transwell membrane inserts and cocultured with human brain...
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| Veröffentlicht in: | Journal of cerebral blood flow and metabolism 2006-02, Vol.26 (2), p.209-217 |
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| creator | Kim, Jeong Ai Tran, Nam D Li, Zhen Yang, Fan Zhou, Weilin Fisher, Mark J |
| description | Pericytes are known to regulate brain capillary endothelial functions. The purpose of this study was to define the hemostatic regulatory role of human brain pericytes. We used blood–brain barrier models consisting of human pericytes grown on transwell membrane inserts and cocultured with human brain microvascular endothelial cells (HBEC), or pericytes grown in direct contact with HBEC. When grown in cocultures in which pericytes were physically separated from endothelial cells, pericytes induced significant changes in endothelial tissue plasminogen activator (tPA) messenger ribonucleic acid (mRNA) and protein: tPA mRNA level was decreased in pericyte cocultures (52% ± 25% of monocultures, P < 0.05) and tPA protein level was decreased (66% ± 23% of monocultures, P < 0.05). Pericyte effects on endothelial fibrinolysis were enhanced when the two cell types were cocultured in direct contact, with tPA protein reduced in cocultures compared with monocultures (25% ± 15% of monocultures, P < 0.05). Endotoxin (lipopolysaccharide (LPS)), used as a standardized stimulus to define brain-specific inflammation-induced change, amplified pericyteinduced enhanced release of the tPA inhibitor plasminogen activator inhibitor-1 (PAI-1); the latter was released by endothelial cells first cocultured with pericytes and then incubated with LPS in the absence of pericytes. Pericytes (in contrast to endothelial cells and astrocytes) were found to be the principal in vitro source of the serpin protease nexin-1 (PN-1), known to have primarily antithrombin effects. These in vitro findings suggest that pericytes negatively regulate brain endothelial cell fibrinolysis, while pericyte expression of PN-1 may provide endogenous anticoagulant activity. |
| doi_str_mv | 10.1038/sj.jcbfm.9600181 |
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The purpose of this study was to define the hemostatic regulatory role of human brain pericytes. We used blood–brain barrier models consisting of human pericytes grown on transwell membrane inserts and cocultured with human brain microvascular endothelial cells (HBEC), or pericytes grown in direct contact with HBEC. When grown in cocultures in which pericytes were physically separated from endothelial cells, pericytes induced significant changes in endothelial tissue plasminogen activator (tPA) messenger ribonucleic acid (mRNA) and protein: tPA mRNA level was decreased in pericyte cocultures (52% ± 25% of monocultures, P < 0.05) and tPA protein level was decreased (66% ± 23% of monocultures, P < 0.05). Pericyte effects on endothelial fibrinolysis were enhanced when the two cell types were cocultured in direct contact, with tPA protein reduced in cocultures compared with monocultures (25% ± 15% of monocultures, P < 0.05). Endotoxin (lipopolysaccharide (LPS)), used as a standardized stimulus to define brain-specific inflammation-induced change, amplified pericyteinduced enhanced release of the tPA inhibitor plasminogen activator inhibitor-1 (PAI-1); the latter was released by endothelial cells first cocultured with pericytes and then incubated with LPS in the absence of pericytes. Pericytes (in contrast to endothelial cells and astrocytes) were found to be the principal in vitro source of the serpin protease nexin-1 (PN-1), known to have primarily antithrombin effects. These in vitro findings suggest that pericytes negatively regulate brain endothelial cell fibrinolysis, while pericyte expression of PN-1 may provide endogenous anticoagulant activity.</description><identifier>ISSN: 0271-678X</identifier><identifier>EISSN: 1559-7016</identifier><identifier>DOI: 10.1038/sj.jcbfm.9600181</identifier><identifier>PMID: 16015279</identifier><identifier>CODEN: JCBMDN</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Amyloid beta-Protein Precursor - genetics ; Amyloid beta-Protein Precursor - metabolism ; Biological and medical sciences ; Brain - blood supply ; Brain - metabolism ; Cells, Cultured ; Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges ; Coculture Techniques - methods ; Endothelial Cells - cytology ; Endothelial Cells - physiology ; Fibrinolysis - physiology ; Fundamental and applied biological sciences. Psychology ; Hemostasis - physiology ; Humans ; Investigative techniques, diagnostic techniques (general aspects) ; Lipopolysaccharides - pharmacology ; Medical sciences ; Nervous system ; Neurology ; Pericytes - cytology ; Pericytes - enzymology ; Pericytes - physiology ; Plasminogen Activator Inhibitor 1 - metabolism ; Protease Nexins ; Receptors, Cell Surface - genetics ; Receptors, Cell Surface - metabolism ; RNA, Messenger - antagonists & inhibitors ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Serpin E2 ; Serpins - genetics ; Serpins - metabolism ; Tissue Plasminogen Activator - antagonists & inhibitors ; Tissue Plasminogen Activator - genetics ; Tissue Plasminogen Activator - metabolism ; Ultrasonic investigative techniques ; Vascular diseases and vascular malformations of the nervous system ; Vertebrates: nervous system and sense organs</subject><ispartof>Journal of cerebral blood flow and metabolism, 2006-02, Vol.26 (2), p.209-217</ispartof><rights>2006 ISCBFM</rights><rights>2006 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Feb 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c522t-3f818877231113535f01e03a2a3ffce71b2b42b5c05a05d19bfc723595ad23083</citedby><cites>FETCH-LOGICAL-c522t-3f818877231113535f01e03a2a3ffce71b2b42b5c05a05d19bfc723595ad23083</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/sj.jcbfm.9600181$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1038/sj.jcbfm.9600181$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,780,784,21819,27924,27925,43621,43622</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17519343$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16015279$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Jeong Ai</creatorcontrib><creatorcontrib>Tran, Nam D</creatorcontrib><creatorcontrib>Li, Zhen</creatorcontrib><creatorcontrib>Yang, Fan</creatorcontrib><creatorcontrib>Zhou, Weilin</creatorcontrib><creatorcontrib>Fisher, Mark J</creatorcontrib><title>Brain endothelial hemostasis regulation by pericytes</title><title>Journal of cerebral blood flow and metabolism</title><addtitle>J Cereb Blood Flow Metab</addtitle><description>Pericytes are known to regulate brain capillary endothelial functions. The purpose of this study was to define the hemostatic regulatory role of human brain pericytes. We used blood–brain barrier models consisting of human pericytes grown on transwell membrane inserts and cocultured with human brain microvascular endothelial cells (HBEC), or pericytes grown in direct contact with HBEC. When grown in cocultures in which pericytes were physically separated from endothelial cells, pericytes induced significant changes in endothelial tissue plasminogen activator (tPA) messenger ribonucleic acid (mRNA) and protein: tPA mRNA level was decreased in pericyte cocultures (52% ± 25% of monocultures, P < 0.05) and tPA protein level was decreased (66% ± 23% of monocultures, P < 0.05). Pericyte effects on endothelial fibrinolysis were enhanced when the two cell types were cocultured in direct contact, with tPA protein reduced in cocultures compared with monocultures (25% ± 15% of monocultures, P < 0.05). Endotoxin (lipopolysaccharide (LPS)), used as a standardized stimulus to define brain-specific inflammation-induced change, amplified pericyteinduced enhanced release of the tPA inhibitor plasminogen activator inhibitor-1 (PAI-1); the latter was released by endothelial cells first cocultured with pericytes and then incubated with LPS in the absence of pericytes. Pericytes (in contrast to endothelial cells and astrocytes) were found to be the principal in vitro source of the serpin protease nexin-1 (PN-1), known to have primarily antithrombin effects. These in vitro findings suggest that pericytes negatively regulate brain endothelial cell fibrinolysis, while pericyte expression of PN-1 may provide endogenous anticoagulant activity.</description><subject>Amyloid beta-Protein Precursor - genetics</subject><subject>Amyloid beta-Protein Precursor - metabolism</subject><subject>Biological and medical sciences</subject><subject>Brain - blood supply</subject><subject>Brain - metabolism</subject><subject>Cells, Cultured</subject><subject>Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges</subject><subject>Coculture Techniques - methods</subject><subject>Endothelial Cells - cytology</subject><subject>Endothelial Cells - physiology</subject><subject>Fibrinolysis - physiology</subject><subject>Fundamental and applied biological sciences. 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Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges</topic><topic>Coculture Techniques - methods</topic><topic>Endothelial Cells - cytology</topic><topic>Endothelial Cells - physiology</topic><topic>Fibrinolysis - physiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hemostasis - physiology</topic><topic>Humans</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Medical sciences</topic><topic>Nervous system</topic><topic>Neurology</topic><topic>Pericytes - cytology</topic><topic>Pericytes - enzymology</topic><topic>Pericytes - physiology</topic><topic>Plasminogen Activator Inhibitor 1 - metabolism</topic><topic>Protease Nexins</topic><topic>Receptors, Cell Surface - genetics</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>RNA, Messenger - antagonists & inhibitors</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Serpin E2</topic><topic>Serpins - genetics</topic><topic>Serpins - metabolism</topic><topic>Tissue Plasminogen Activator - antagonists & inhibitors</topic><topic>Tissue Plasminogen Activator - genetics</topic><topic>Tissue Plasminogen Activator - metabolism</topic><topic>Ultrasonic investigative techniques</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Jeong Ai</creatorcontrib><creatorcontrib>Tran, Nam D</creatorcontrib><creatorcontrib>Li, Zhen</creatorcontrib><creatorcontrib>Yang, Fan</creatorcontrib><creatorcontrib>Zhou, Weilin</creatorcontrib><creatorcontrib>Fisher, Mark J</creatorcontrib><collection>Pascal-Francis</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>ProQuest Pharma Collection</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>Biological Science 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 China</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cerebral blood flow and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Jeong Ai</au><au>Tran, Nam D</au><au>Li, Zhen</au><au>Yang, Fan</au><au>Zhou, Weilin</au><au>Fisher, Mark J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Brain endothelial hemostasis regulation by pericytes</atitle><jtitle>Journal of cerebral blood flow and metabolism</jtitle><addtitle>J Cereb Blood Flow Metab</addtitle><date>2006-02-01</date><risdate>2006</risdate><volume>26</volume><issue>2</issue><spage>209</spage><epage>217</epage><pages>209-217</pages><issn>0271-678X</issn><eissn>1559-7016</eissn><coden>JCBMDN</coden><abstract>Pericytes are known to regulate brain capillary endothelial functions. The purpose of this study was to define the hemostatic regulatory role of human brain pericytes. We used blood–brain barrier models consisting of human pericytes grown on transwell membrane inserts and cocultured with human brain microvascular endothelial cells (HBEC), or pericytes grown in direct contact with HBEC. When grown in cocultures in which pericytes were physically separated from endothelial cells, pericytes induced significant changes in endothelial tissue plasminogen activator (tPA) messenger ribonucleic acid (mRNA) and protein: tPA mRNA level was decreased in pericyte cocultures (52% ± 25% of monocultures, P < 0.05) and tPA protein level was decreased (66% ± 23% of monocultures, P < 0.05). Pericyte effects on endothelial fibrinolysis were enhanced when the two cell types were cocultured in direct contact, with tPA protein reduced in cocultures compared with monocultures (25% ± 15% of monocultures, P < 0.05). Endotoxin (lipopolysaccharide (LPS)), used as a standardized stimulus to define brain-specific inflammation-induced change, amplified pericyteinduced enhanced release of the tPA inhibitor plasminogen activator inhibitor-1 (PAI-1); the latter was released by endothelial cells first cocultured with pericytes and then incubated with LPS in the absence of pericytes. Pericytes (in contrast to endothelial cells and astrocytes) were found to be the principal in vitro source of the serpin protease nexin-1 (PN-1), known to have primarily antithrombin effects. These in vitro findings suggest that pericytes negatively regulate brain endothelial cell fibrinolysis, while pericyte expression of PN-1 may provide endogenous anticoagulant activity.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>16015279</pmid><doi>10.1038/sj.jcbfm.9600181</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Amyloid beta-Protein Precursor - genetics Amyloid beta-Protein Precursor - metabolism Biological and medical sciences Brain - blood supply Brain - metabolism Cells, Cultured Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges Coculture Techniques - methods Endothelial Cells - cytology Endothelial Cells - physiology Fibrinolysis - physiology Fundamental and applied biological sciences. Psychology Hemostasis - physiology Humans Investigative techniques, diagnostic techniques (general aspects) Lipopolysaccharides - pharmacology Medical sciences Nervous system Neurology Pericytes - cytology Pericytes - enzymology Pericytes - physiology Plasminogen Activator Inhibitor 1 - metabolism Protease Nexins Receptors, Cell Surface - genetics Receptors, Cell Surface - metabolism RNA, Messenger - antagonists & inhibitors RNA, Messenger - genetics RNA, Messenger - metabolism Serpin E2 Serpins - genetics Serpins - metabolism Tissue Plasminogen Activator - antagonists & inhibitors Tissue Plasminogen Activator - genetics Tissue Plasminogen Activator - metabolism Ultrasonic investigative techniques Vascular diseases and vascular malformations of the nervous system Vertebrates: nervous system and sense organs |
| title | Brain endothelial hemostasis regulation by pericytes |
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