Tamoxifen inhibits endothelial cell proliferation and attenuates VEGF-mediated angiogenesis and migration in vivo

2001 ◽  
Vol 27 (8) ◽  
pp. 714-718 ◽  
Author(s):  
D.A McNamara ◽  
J Harmey ◽  
J.H Wang ◽  
E Kay ◽  
T.N Walsh ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Endothelial Cell Proliferation ◽  
And Migration

scholarly journals N-acetyl-seryl-aspartyl-lysyl-proline stimulates angiogenesis in vitro and in vivo

2004 ◽  
Vol 287 (5) ◽  
pp. H2099-H2105 ◽  
Author(s):  
Dahai Wang ◽  
Oscar A. Carretero ◽  
Xiao-Yi Yang ◽  
Nour-Eddine Rhaleb ◽  
Yun-He Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Capillary Density ◽  
Tube Formation ◽  
Endothelial Cell Proliferation ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), a natural inhibitor of pluripotent hematopoietic stem cell proliferation, has been suggested as capable of promoting an angiogenic response. We studied whether Ac-SDKP stimulates endothelial cell proliferation, migration, and tube formation; enhances angiogenic response in the rat cornea after implantation of a tumor spheroid; and increases capillary density in rat hearts with myocardial infarction (MI). In vitro, an immortal BALB/c mouse aortic endothelial 22106 cell line was used to determine the effects of Ac-SDKP on endothelial cell proliferation and migration and tube formation. In vivo, a 9L-gliosarcoma cell spheroid (250–300 μm in diameter) was implanted in the rat cornea and vehicle or Ac-SDKP (800 μg·kg−1·day−1ip) infused via osmotic minipump. Myocardial capillary density was studied in rats with MI given either vehicle or Ac-SDKP. We found that Ac-SDKP 1) stimulated endothelial cell proliferation and migration and tube formation in a dose-dependent manner, 2) enhanced corneal neovascularization, and 3) increased myocardial capillary density. Endothelial cell proliferation and angiogenesis stimulated by Ac-SDKP could be beneficial in cardiovascular diseases such as hypertension and MI. Furthermore, because Ac-SDKP is mainly cleaved by ACE, it may partially mediate the cardioprotective effect of ACE inhibitors.

scholarly journals Des-γ-carboxyl Prothrombin-promoted Vascular Endothelial Cell Proliferation and Migration

2007 ◽  
Vol 282 (12) ◽  
pp. 8741-8748 ◽  
Author(s):  
Tatsuya Fujikawa ◽  
Hidenori Shiraha ◽  
Naoki Ueda ◽  
Nobuyuki Takaoka ◽  
Yutaka Nakanishi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Endothelial Cell Proliferation ◽  
Vascular Endothelial ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Angiopoietin-1 promotes endothelial cell proliferation and migration through AP-1–dependent autocrine production of interleukin-8

Blood ◽  
2008 ◽  
Vol 111 (8) ◽  
pp. 4145-4154 ◽  
Author(s):  
Nelly A. Abdel-Malak ◽  
Coimbatore B. Srikant ◽  
Arnold S. Kristof ◽  
Sheldon A. Magder ◽  
John A. Di Battista ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Interleukin 8 ◽  
Endothelial Cell Migration ◽  
Endothelial Cell Proliferation ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration ◽  
Angiopoietin 1

Abstract Angiopoietin-1 (Ang-1), ligand for the endothelial cell–specific Tie-2 receptors, promotes migration and proliferation of endothelial cells, however, whether these effects are promoted through the release of a secondary mediator remains unclear. In this study, we assessed whether Ang-1 promotes endothelial cell migration and proliferation through the release of interleukin-8 (IL-8). Ang-1 elicited in human umbilical vein endothelial cells (HUVECs) a dose- and time-dependent increase in IL-8 production as a result of induction of mRNA and enhanced mRNA stability of IL-8 transcripts. IL-8 production is also elevated in HUVECs transduced with retroviruses expressing Ang-1. Neutralization of IL-8 in these cells with a specific antibody significantly attenuated proliferation and migration and induced caspase-3 activation. Exposure to Ang-1 triggered a significant increase in DNA binding of activator protein-1 (AP-1) to a relatively short fragment of IL-8 promoter. Upstream from the AP-1 complex, up-regulation of IL-8 transcription by Ang-1 was mediated through the Erk1/2, SAPK/JNK, and PI-3 kinase pathways, which triggered c-Jun phosphorylation on Ser63 and Ser73. These results suggest that promotion of endothelial migration and proliferation by Ang-1 is mediated, in part, through the production of IL-8, which acts in an autocrine fashion to suppress apoptosis and facilitate cell proliferation and migration.

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