title: [Inhibitory effect of suberoylanilide hydroxamic acid on angiogenesis and its molecular mechanism].
abstract: OBJECTIVE
  To study the effect of histone deacetylase inhibitor (HDACi), suberoylanilide hydroxamic acid (SAHA) on the angiogenesis and the biological characteristics of human umbilical vein endothelial cells (HUVECs).
  
  
  METHODS
  The proliferation of HUVECs affected by SAHA was investigated by CCK-8. After treated with 15 μmol/L SAHA for 48 hours, HUVECs underwent the Transwell (TM); assay to observe the migration, the Matrigel angiogenesis assay in vitro to test the ability of tube formation, Western blotting to evaluate the change of vascular endothelial growth factor (VEGF)-induced signaling pathway, and the Matrigel-based tube formation assay in vivo to observe the new formed vessel in matrigel plug, thereby evaluating the effect of SAHA on the angiogenesis in mice.
  
  
  RESULTS
  Compared with the control group, SAHA significantly suppressed HUVECs proliferation in a dose-dependent and time-dependent manner. The number of migrated HUVECs was significantly reduced after the treatment of 15 μmol/L SAHA for 48 hours. The Matrigel angiogenesis in vitro suggested that the capillary-like tube formation in the SAHA treated group was less than that in the control group. Western blotting demonstrated that SAHA inhibited the VEGF-induced signaling pathway. The number of new formed vessels in the Matrigel plug in the SAHA treated group was less than that in the control group.
  
  
  CONCLUSIONS
  SAHA suppresses the proliferation of HUVECs and the angiogenensis in vivo and in vitro. The potential mechanism of the inhibition may be SAHA blockage of the VEGF-induced signaling pathway.
authors.affiliation: Department of Physiopathology, Institute of Tissue and Cell Engineering, Chongqing Medical University, Chongqing 400016, China.
authors.forename: Nana
authors.initials: N
authors.lastname: Wang
authors.affiliation: Department of Physiopathology, Institute of Tissue and Cell Engineering, Chongqing Medical University, Chongqing 400016, China.
authors.forename: Linbo
authors.initials: L
authors.lastname: Chen
authors.affiliation: Department of Physiopathology, Institute of Tissue and Cell Engineering, Chongqing Medical University, Chongqing 400016, China.
authors.forename: Li
authors.initials: L
authors.lastname: Zhang
authors.affiliation: Department of Physiopathology, Institute of Tissue and Cell Engineering, Chongqing Medical University, Chongqing 400016, China.
authors.forename: Rong
authors.initials: R
authors.lastname: Jiang
authors.affiliation: Experimental Teaching Center, Chongqing Medical University, Chongqing 400016, China.
authors.forename: Li
authors.initials: L
authors.lastname: Chen
authors.affiliation: Department of Physiopathology, Institute of Tissue and Cell Engineering, Chongqing Medical University, Chongqing 400016, China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Shen
mesh_terms: D020533:Angiogenesis Inhibitors / Q000494:pharmacology*; D000818:Animals; D002465:Cell Movement / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D056572:Histone Deacetylase Inhibitors / Q000494:pharmacology*; D006801:Humans; D006877:Hydroxamic Acids / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018919:Neovascularization, Physiologic / Q000187:drug effects; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors; D000077337:Vorinostat
chemical_list: D020533:Angiogenesis Inhibitors; D056572:Histone Deacetylase Inhibitors; D006877:Hydroxamic Acids; D042461:Vascular Endothelial Growth Factor A; D000077337:Vorinostat