title: Control of angiogenesis by inhibitor of phospholipase A2.
abstract: OBJECTIVE
  To investigate the potential effects of angiogenic process by secretory phospholipase A2 (sPLA2) inhibitor-HyPE (linking N-derivatized phosphatidyl-ethanolamine to hyaluronic 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 hy 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 2.5 ng/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.
authors.affiliation: Beijing Chaoyang Hospital, Capital University of Medical Sciences, Beijing 100020. wenming_chen@yahoo.com
authors.forename: Wenming
authors.initials: W
authors.lastname: Chen
authors.forename: Lihong
authors.initials: L
authors.lastname: Li
authors.forename: Jiazhi
authors.initials: J
authors.lastname: Zhu
authors.forename: Jinwei
authors.initials: J
authors.lastname: Liu
authors.forename: Jeannette
authors.initials: J
authors.lastname: Soria
authors.forename: Claudine
authors.initials: C
authors.lastname: Soria
authors.forename: Saul
authors.initials: S
authors.lastname: Yedgar
mesh_terms: D001854:Bone Marrow Cells / Q000166:cytology; D002196:Capillaries / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects; D002465:Cell Movement / Q000187:drug effects; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000166:cytology; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D016222:Fibroblast Growth Factor 2 / Q000037:antagonists & inhibitors; D006801:Humans; D006820:Hyaluronic Acid / Q000494:pharmacology; D009389:Neovascularization, Pathologic / Q000473:pathology*; D053683:Oncostatin M; D010455:Peptides / Q000037:antagonists & inhibitors; D010714:Phosphatidylethanolamines / Q000494:pharmacology; D010741:Phospholipases A / Q000037:antagonists & inhibitors*; D054467:Phospholipases A2; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors
chemical_list: D004791:Enzyme Inhibitors; C508351:OSM protein, human; D010455:Peptides; D010714:Phosphatidylethanolamines; D042461:Vascular Endothelial Growth Factor A; D016222:Fibroblast Growth Factor 2; D053683:Oncostatin M; D006820:Hyaluronic Acid; D010741:Phospholipases A; D054467:Phospholipases A2