Inhibition of Angiogenic Properties of Brain Endothelial Cells by Platelet-Derived Sphingosine-1-Phosphate
The platelet-derived lysophospholipid sphingosine-1-phosphate (S1P) is present in blood plasma and is one of the most potent growth factors displaying proangiogenic activity towards endothelial cells (EC) derived from various tissues. The paracrine regulation of brain angiogenesis by platelet-derive...
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description | The platelet-derived lysophospholipid sphingosine-1-phosphate (S1P) is present in blood plasma and is one of the most potent growth factors displaying proangiogenic activity towards endothelial cells (EC) derived from various tissues. The paracrine regulation of brain angiogenesis by platelet-derived growth factors is, however, poorly understood. In the present study, we assessed the role of S1P on brain EC migration and tubulogenesis, using rat brain-derived (RBE4) EC as an in vitro model. We show that S1P inhibits brain EC migration and tubulogenesis, while it displays proangiogenic activity towards noncerebral EC. Overexpression of the S1P receptor S1P-1 in RBE4 cells potentiated all of the S1P-mediated events. We also show that the lack of expression of MT1-MMP, a membrane-bound matrix metalloproteinase that is thought to cooperate with S1P in tubulogenic processes, may explain the antiangiogenic activity of S1P on brain vasculature. Altogether our results support the hypothesis of a tissue-specific, antiangiogenic role of S1P in the brain, which may help to stabilize the cerebral vasculature and thus have crucial impact on the setting and regulation of normal brain vascularization. |
doi_str_mv | 10.1038/sj.jcbfm.9600117 |
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The paracrine regulation of brain angiogenesis by platelet-derived growth factors is, however, poorly understood. In the present study, we assessed the role of S1P on brain EC migration and tubulogenesis, using rat brain-derived (RBE4) EC as an in vitro model. We show that S1P inhibits brain EC migration and tubulogenesis, while it displays proangiogenic activity towards noncerebral EC. Overexpression of the S1P receptor S1P-1 in RBE4 cells potentiated all of the S1P-mediated events. We also show that the lack of expression of MT1-MMP, a membrane-bound matrix metalloproteinase that is thought to cooperate with S1P in tubulogenic processes, may explain the antiangiogenic activity of S1P on brain vasculature. 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Drug treatments ; Rats ; Reverse Transcriptase Polymerase Chain Reaction ; RNA - biosynthesis ; RNA - isolation & purification ; Sphingosine - analogs & derivatives ; Sphingosine - blood ; Sphingosine - pharmacology ; Transfection ; Ultrasonic investigative techniques ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Journal of cerebral blood flow and metabolism, 2005-09, Vol.25 (9), p.1171-1182</ispartof><rights>2005 ISCBFM</rights><rights>2005 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Sep 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c434t-60751d42bd8dd1734615c66f722202107eacf33210868bf8b29258cfb21931d23</citedby><cites>FETCH-LOGICAL-c434t-60751d42bd8dd1734615c66f722202107eacf33210868bf8b29258cfb21931d23</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.9600117$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1038/sj.jcbfm.9600117$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,777,781,21800,27905,27906,43602,43603</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17084898$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15829917$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pilorget, Anthony</creatorcontrib><creatorcontrib>Annabi, Borhane</creatorcontrib><creatorcontrib>Bouzeghrane, Fatiha</creatorcontrib><creatorcontrib>Marvaldi, Jacques</creatorcontrib><creatorcontrib>Luis, José</creatorcontrib><creatorcontrib>Béliveau, Richard</creatorcontrib><title>Inhibition of Angiogenic Properties of Brain Endothelial Cells by Platelet-Derived Sphingosine-1-Phosphate</title><title>Journal of cerebral blood flow and metabolism</title><addtitle>J Cereb Blood Flow Metab</addtitle><description>The platelet-derived lysophospholipid sphingosine-1-phosphate (S1P) is present in blood plasma and is one of the most potent growth factors displaying proangiogenic activity towards endothelial cells (EC) derived from various tissues. The paracrine regulation of brain angiogenesis by platelet-derived growth factors is, however, poorly understood. In the present study, we assessed the role of S1P on brain EC migration and tubulogenesis, using rat brain-derived (RBE4) EC as an in vitro model. We show that S1P inhibits brain EC migration and tubulogenesis, while it displays proangiogenic activity towards noncerebral EC. Overexpression of the S1P receptor S1P-1 in RBE4 cells potentiated all of the S1P-mediated events. We also show that the lack of expression of MT1-MMP, a membrane-bound matrix metalloproteinase that is thought to cooperate with S1P in tubulogenic processes, may explain the antiangiogenic activity of S1P on brain vasculature. 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Drug treatments</topic><topic>Rats</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA - biosynthesis</topic><topic>RNA - isolation & purification</topic><topic>Sphingosine - analogs & derivatives</topic><topic>Sphingosine - blood</topic><topic>Sphingosine - pharmacology</topic><topic>Transfection</topic><topic>Ultrasonic investigative techniques</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pilorget, Anthony</creatorcontrib><creatorcontrib>Annabi, Borhane</creatorcontrib><creatorcontrib>Bouzeghrane, Fatiha</creatorcontrib><creatorcontrib>Marvaldi, Jacques</creatorcontrib><creatorcontrib>Luis, José</creatorcontrib><creatorcontrib>Béliveau, Richard</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>Pilorget, Anthony</au><au>Annabi, Borhane</au><au>Bouzeghrane, Fatiha</au><au>Marvaldi, Jacques</au><au>Luis, José</au><au>Béliveau, Richard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of Angiogenic Properties of Brain Endothelial Cells by Platelet-Derived Sphingosine-1-Phosphate</atitle><jtitle>Journal of cerebral blood flow and metabolism</jtitle><addtitle>J Cereb Blood Flow Metab</addtitle><date>2005-09-01</date><risdate>2005</risdate><volume>25</volume><issue>9</issue><spage>1171</spage><epage>1182</epage><pages>1171-1182</pages><issn>0271-678X</issn><eissn>1559-7016</eissn><coden>JCBMDN</coden><abstract>The platelet-derived lysophospholipid sphingosine-1-phosphate (S1P) is present in blood plasma and is one of the most potent growth factors displaying proangiogenic activity towards endothelial cells (EC) derived from various tissues. The paracrine regulation of brain angiogenesis by platelet-derived growth factors is, however, poorly understood. In the present study, we assessed the role of S1P on brain EC migration and tubulogenesis, using rat brain-derived (RBE4) EC as an in vitro model. We show that S1P inhibits brain EC migration and tubulogenesis, while it displays proangiogenic activity towards noncerebral EC. Overexpression of the S1P receptor S1P-1 in RBE4 cells potentiated all of the S1P-mediated events. We also show that the lack of expression of MT1-MMP, a membrane-bound matrix metalloproteinase that is thought to cooperate with S1P in tubulogenic processes, may explain the antiangiogenic activity of S1P on brain vasculature. Altogether our results support the hypothesis of a tissue-specific, antiangiogenic role of S1P in the brain, which may help to stabilize the cerebral vasculature and thus have crucial impact on the setting and regulation of normal brain vascularization.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>15829917</pmid><doi>10.1038/sj.jcbfm.9600117</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Biological and medical sciences Blood Platelets - chemistry Blotting, Western Cell Adhesion Cell Differentiation - drug effects Cell Movement Cells, Cultured Culture Media DNA, Complementary - biosynthesis DNA, Complementary - genetics Endothelial Cells - drug effects Endothelial Cells - ultrastructure Growth Substances - pharmacology Humans Investigative techniques, diagnostic techniques (general aspects) Lysophospholipids - blood Lysophospholipids - pharmacology Matrix Metalloproteinase 1 - metabolism Medical sciences Neovascularization, Physiologic - drug effects Nervous system Neurology Neuropharmacology Neuroprotective agent Oligonucleotides, Antisense - pharmacology Pharmacology. Drug treatments Rats Reverse Transcriptase Polymerase Chain Reaction RNA - biosynthesis RNA - isolation & purification Sphingosine - analogs & derivatives Sphingosine - blood Sphingosine - pharmacology Transfection Ultrasonic investigative techniques Vascular diseases and vascular malformations of the nervous system |
title | Inhibition of Angiogenic Properties of Brain Endothelial Cells by Platelet-Derived Sphingosine-1-Phosphate |
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