CONTROL OF ANGIOGENESIS BY INHIBITOR OF PHOSPHOLIPASE A2
Objective To investigate the potential effects of angiogenic process by secretory phospholipase A2 (sPLA2) inhibitor-HyPE (linking N-derivatized phosphatidyl-ethanolamine to hyaluronie acid) on human bone marrow endothelial cell line (HBME-1). Methods In order to examine the suppressing effects of H...
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| Veröffentlicht in: | Chinese medical sciences journal 2004-03, Vol.19 (1), p.6-12 |
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| creator | 陈文明 李利红 朱嘉芷 刘晋玮 SoriaJeannette SoriaClaudine YedgarSaul |
| description | Objective To investigate the potential effects of angiogenic process by secretory phospholipase A2 (sPLA2) inhibitor-HyPE (linking N-derivatized phosphatidyl-ethanolamine to hyaluronie acid) on human bone marrow endothelial cell line (HBME-1). Methods In order to examine the suppressing effects of HyPE on HBME-1 proliferation, migration, and capillary-like tube formation, HBME-1 were activated by angiogenic factor, specifically by basic fibroblast growth factor (b-FGF), vascular endothelial growth factor (VEGF), and oncostatin M (OSM) (at a final concentration of 25, 20, and 2.5ng/mL, respectively), then HBME-1 proliferation, migration, and tube formation were studied in the absence or presence of HyPE. HBME-1 tube formation was specially analyzed in fibrin gel. Results HyPE effectively inhibited HBME-1 proliferation and migration as a dose-dependent manner,whatever HBME-1 were grown in the control culture medium or stimulated with b-FGF, VEGF, or OSM. In fibrin, the formations of HBME-1 derived tube-like structures were enhanced by all angiogenic factors, but these were strongly suppressed by HyPE. Conclusions The results support the involvement of sPLA2 in angiogenesis. It is proposed that sPLA2 inhibitor introduces a novel approach in the control of cancer development. |
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Methods In order to examine the suppressing effects of HyPE on HBME-1 proliferation, migration, and capillary-like tube formation, HBME-1 were activated by angiogenic factor, specifically by basic fibroblast growth factor (b-FGF), vascular endothelial growth factor (VEGF), and oncostatin M (OSM) (at a final concentration of 25, 20, and 2.5ng/mL, respectively), then HBME-1 proliferation, migration, and tube formation were studied in the absence or presence of HyPE. HBME-1 tube formation was specially analyzed in fibrin gel. Results HyPE effectively inhibited HBME-1 proliferation and migration as a dose-dependent manner,whatever HBME-1 were grown in the control culture medium or stimulated with b-FGF, VEGF, or OSM. In fibrin, the formations of HBME-1 derived tube-like structures were enhanced by all angiogenic factors, but these were strongly suppressed by HyPE. Conclusions The results support the involvement of sPLA2 in angiogenesis. It is proposed that sPLA2 inhibitor introduces a novel approach in the control of cancer development.</description><identifier>ISSN: 1001-9294</identifier><identifier>PMID: 15104217</identifier><language>eng</language><publisher>China: Beijing Chaoyang Hospital, Capital University of Medical Sciences, Beijing 100020%Hotel Dieu, Paris 75181, France%Laboratoire Difema, Faculte de Medecine et de Phamacie, Rouen 76000, France%Hadassah Hospital, Jerusalem 45120, Israel</publisher><subject>Bone Marrow Cells - cytology ; Capillaries - drug effects ; Cell Division - drug effects ; Cell Movement - drug effects ; Cells, Cultured ; Endothelial Cells - cytology ; Enzyme Inhibitors - pharmacology ; Fibroblast Growth Factor 2 - antagonists & inhibitors ; Humans ; Hyaluronic Acid - pharmacology ; Neovascularization, Pathologic - pathology ; Oncostatin M ; Peptides - antagonists & inhibitors ; Phosphatidylethanolamines - pharmacology ; Phospholipases A - antagonists & inhibitors ; Phospholipases A2 ; Vascular Endothelial Growth Factor A - antagonists & inhibitors ; 磷脂酶A2 ; 细胞因子 ; 细胞增殖 ; 肿瘤病理学 ; 血管内皮细胞 ; 血管生成</subject><ispartof>Chinese medical sciences journal, 2004-03, Vol.19 (1), p.6-12</ispartof><rights>Copyright © Wanfang Data Co. Ltd. All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/86798X/86798X.jpg</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15104217$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>陈文明 李利红 朱嘉芷 刘晋玮 SoriaJeannette SoriaClaudine YedgarSaul</creatorcontrib><title>CONTROL OF ANGIOGENESIS BY INHIBITOR OF PHOSPHOLIPASE A2</title><title>Chinese medical sciences journal</title><addtitle>Chinese Medical Sciences Journal</addtitle><description>Objective To investigate the potential effects of angiogenic process by secretory phospholipase A2 (sPLA2) inhibitor-HyPE (linking N-derivatized phosphatidyl-ethanolamine to hyaluronie acid) on human bone marrow endothelial cell line (HBME-1). Methods In order to examine the suppressing effects of HyPE on HBME-1 proliferation, migration, and capillary-like tube formation, HBME-1 were activated by angiogenic factor, specifically by basic fibroblast growth factor (b-FGF), vascular endothelial growth factor (VEGF), and oncostatin M (OSM) (at a final concentration of 25, 20, and 2.5ng/mL, respectively), then HBME-1 proliferation, migration, and tube formation were studied in the absence or presence of HyPE. HBME-1 tube formation was specially analyzed in fibrin gel. Results HyPE effectively inhibited HBME-1 proliferation and migration as a dose-dependent manner,whatever HBME-1 were grown in the control culture medium or stimulated with b-FGF, VEGF, or OSM. In fibrin, the formations of HBME-1 derived tube-like structures were enhanced by all angiogenic factors, but these were strongly suppressed by HyPE. Conclusions The results support the involvement of sPLA2 in angiogenesis. It is proposed that sPLA2 inhibitor introduces a novel approach in the control of cancer development.</description><subject>Bone Marrow Cells - cytology</subject><subject>Capillaries - drug effects</subject><subject>Cell Division - drug effects</subject><subject>Cell Movement - drug effects</subject><subject>Cells, Cultured</subject><subject>Endothelial Cells - cytology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Fibroblast Growth Factor 2 - antagonists & inhibitors</subject><subject>Humans</subject><subject>Hyaluronic Acid - pharmacology</subject><subject>Neovascularization, Pathologic - pathology</subject><subject>Oncostatin M</subject><subject>Peptides - antagonists & inhibitors</subject><subject>Phosphatidylethanolamines - pharmacology</subject><subject>Phospholipases A - antagonists & inhibitors</subject><subject>Phospholipases A2</subject><subject>Vascular Endothelial Growth Factor A - antagonists & inhibitors</subject><subject>磷脂酶A2</subject><subject>细胞因子</subject><subject>细胞增殖</subject><subject>肿瘤病理学</subject><subject>血管内皮细胞</subject><subject>血管生成</subject><issn>1001-9294</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kM1ugzAQhDm0atK0r1DRS3tCWhsbzJFEJEFCEIX00JNlGzsl5SeBoKpvX6Kkh9WOtJ9mNHtnTREAcgIckIn12PcHAPAQIw_WBFEEBCN_arFFlu62WWJnSztMV3G2itIoj3N7_mnH6Tqex7tsezlu1lk-ThJvwjyyQ_xk3RtR9fr5tmfWxzLaLdZOkq3iRZg4CjHADlNUK2ooM0YiCobRAICASz2JkAKQ2ADxQZPC96TrFoh4Qko1SuZJVgh3Zr1ffX9EY0Sz54d26Joxkau6P3CNL3ZjUTySb1fy2LWnQfdnXpe90lUlGt0OPfcRoyTAF_DlBg6y1gU_dmUtul_-_5UReL0C6qtt9qdyTJVCfZuy0jzwKCKUun9XK2B0</recordid><startdate>200403</startdate><enddate>200403</enddate><creator>陈文明 李利红 朱嘉芷 刘晋玮 SoriaJeannette SoriaClaudine YedgarSaul</creator><general>Beijing Chaoyang Hospital, Capital University of Medical Sciences, Beijing 100020%Hotel Dieu, Paris 75181, France%Laboratoire Difema, Faculte de Medecine et de Phamacie, Rouen 76000, France%Hadassah Hospital, Jerusalem 45120, Israel</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W91</scope><scope>~WA</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>2B.</scope><scope>4A8</scope><scope>92I</scope><scope>93N</scope><scope>PSX</scope><scope>TCJ</scope></search><sort><creationdate>200403</creationdate><title>CONTROL OF ANGIOGENESIS BY INHIBITOR OF PHOSPHOLIPASE A2</title><author>陈文明 李利红 朱嘉芷 刘晋玮 SoriaJeannette SoriaClaudine YedgarSaul</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1802-8c5ec5f58ffb150f8590040356b11c00b2f0470e4d76b33d146abbcb3386b8da3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Bone Marrow Cells - cytology</topic><topic>Capillaries - drug effects</topic><topic>Cell Division - drug effects</topic><topic>Cell Movement - drug effects</topic><topic>Cells, Cultured</topic><topic>Endothelial Cells - cytology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Fibroblast Growth Factor 2 - antagonists & inhibitors</topic><topic>Humans</topic><topic>Hyaluronic Acid - pharmacology</topic><topic>Neovascularization, Pathologic - pathology</topic><topic>Oncostatin M</topic><topic>Peptides - antagonists & inhibitors</topic><topic>Phosphatidylethanolamines - pharmacology</topic><topic>Phospholipases A - antagonists & inhibitors</topic><topic>Phospholipases A2</topic><topic>Vascular Endothelial Growth Factor A - antagonists & inhibitors</topic><topic>磷脂酶A2</topic><topic>细胞因子</topic><topic>细胞增殖</topic><topic>肿瘤病理学</topic><topic>血管内皮细胞</topic><topic>血管生成</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>陈文明 李利红 朱嘉芷 刘晋玮 SoriaJeannette SoriaClaudine YedgarSaul</creatorcontrib><collection>中文科技期刊数据库</collection><collection>中文科技期刊数据库-CALIS站点</collection><collection>中文科技期刊数据库-7.0平台</collection><collection>中文科技期刊数据库-医药卫生</collection><collection>中文科技期刊数据库- 镜像站点</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>Wanfang Data Journals - Hong Kong</collection><collection>WANFANG Data Centre</collection><collection>Wanfang Data Journals</collection><collection>万方数据期刊 - 香港版</collection><collection>China Online Journals (COJ)</collection><collection>China Online Journals (COJ)</collection><jtitle>Chinese medical sciences journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>陈文明 李利红 朱嘉芷 刘晋玮 SoriaJeannette SoriaClaudine YedgarSaul</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CONTROL OF ANGIOGENESIS BY INHIBITOR OF PHOSPHOLIPASE A2</atitle><jtitle>Chinese medical sciences journal</jtitle><addtitle>Chinese Medical Sciences Journal</addtitle><date>2004-03</date><risdate>2004</risdate><volume>19</volume><issue>1</issue><spage>6</spage><epage>12</epage><pages>6-12</pages><issn>1001-9294</issn><abstract>Objective To investigate the potential effects of angiogenic process by secretory phospholipase A2 (sPLA2) inhibitor-HyPE (linking N-derivatized phosphatidyl-ethanolamine to hyaluronie acid) on human bone marrow endothelial cell line (HBME-1). Methods In order to examine the suppressing effects of HyPE on HBME-1 proliferation, migration, and capillary-like tube formation, HBME-1 were activated by angiogenic factor, specifically by basic fibroblast growth factor (b-FGF), vascular endothelial growth factor (VEGF), and oncostatin M (OSM) (at a final concentration of 25, 20, and 2.5ng/mL, respectively), then HBME-1 proliferation, migration, and tube formation were studied in the absence or presence of HyPE. HBME-1 tube formation was specially analyzed in fibrin gel. Results HyPE effectively inhibited HBME-1 proliferation and migration as a dose-dependent manner,whatever HBME-1 were grown in the control culture medium or stimulated with b-FGF, VEGF, or OSM. In fibrin, the formations of HBME-1 derived tube-like structures were enhanced by all angiogenic factors, but these were strongly suppressed by HyPE. Conclusions The results support the involvement of sPLA2 in angiogenesis. It is proposed that sPLA2 inhibitor introduces a novel approach in the control of cancer development.</abstract><cop>China</cop><pub>Beijing Chaoyang Hospital, Capital University of Medical Sciences, Beijing 100020%Hotel Dieu, Paris 75181, France%Laboratoire Difema, Faculte de Medecine et de Phamacie, Rouen 76000, France%Hadassah Hospital, Jerusalem 45120, Israel</pub><pmid>15104217</pmid><tpages>7</tpages></addata></record> |
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| subjects | Bone Marrow Cells - cytology Capillaries - drug effects Cell Division - drug effects Cell Movement - drug effects Cells, Cultured Endothelial Cells - cytology Enzyme Inhibitors - pharmacology Fibroblast Growth Factor 2 - antagonists & inhibitors Humans Hyaluronic Acid - pharmacology Neovascularization, Pathologic - pathology Oncostatin M Peptides - antagonists & inhibitors Phosphatidylethanolamines - pharmacology Phospholipases A - antagonists & inhibitors Phospholipases A2 Vascular Endothelial Growth Factor A - antagonists & inhibitors 磷脂酶A2 细胞因子 细胞增殖 肿瘤病理学 血管内皮细胞 血管生成 |
| title | CONTROL OF ANGIOGENESIS BY INHIBITOR OF PHOSPHOLIPASE A2 |
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