Angiostatin-induced inhibition of endothelial cell proliferation/apoptosis is associated with the down-regulation of cell cycle regulatory protein cdk5

2004 ◽  
Vol 91 (2) ◽  
pp. 398-409 ◽  
Author(s):  
Meena R. Sharma ◽  
George P. Tuszynski ◽  
Mahesh C. Sharma
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Endothelial Cell ◽  
Regulatory Protein ◽  
Endothelial Cell Proliferation ◽  
Down Regulation ◽  
Cell Cycle Regulatory Protein ◽  
Regulation Of Cell Cycle

scholarly journals The GPER1 Agonist G-1 Attenuates Endothelial Cell Proliferation by Inhibiting DNA Synthesis and Accumulating Cells in the S and G2 Phases of the Cell Cycle

2011 ◽  
Vol 48 (4) ◽  
pp. 327-335 ◽  
Author(s):  
Anders Holm ◽  
Bo Baldetorp ◽  
Björn Olde ◽  
L.M. Fredrik Leeb-Lundberg ◽  
Bengt-Olof Nilsson
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Endothelial Cell ◽  
Dna Synthesis ◽  
Endothelial Cell Proliferation

Inhibition of Human Umbilical Vein Endothelial Cell Proliferation by the CXC Chemokine, Platelet Factor 4 (PF4), Is Associated With Impaired Downregulation of p21Cip1/WAF1

Blood ◽  
1999 ◽  
Vol 93 (1) ◽  
pp. 25-33 ◽  
Author(s):  
Grazia Gentilini ◽  
Nancy E. Kirschbaum ◽  
James A. Augustine ◽  
Richard H. Aster ◽  
Gian Paolo Visentin
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Cyclin E ◽  
Endothelial Cell Proliferation ◽  
Cyclin Dependent Kinase ◽  
Platelet Factor ◽  
Human Umbilical Vein ◽  
Cdk2 Activity

Human PF4 is a heparin-binding chemokine known to be capable of inhibiting endothelial cell proliferation and angiogenesis. To explore the biological mechanisms responsible for this action, we investigated the effect of PF4 on epidermal growth factor (EGF)-stimulated human umbilical vein endothelial cells (HUVEC), a model system in which stimulation is essentially independent of interaction with cell-surface glycosaminoglycans. Based on previous findings that PF4 blocks endothelial cell cycle entry and progression into S phase, we studied the molecular mechanism(s) of PF4 interference with cell cycle machinery. PF4 treatment of EGF-stimulated HUVEC caused a decrease in cyclin E–cyclin-dependent kinase 2 (cdk2) activity with resulting attenuation of retinoblastoma protein phosphorylation. PF4-dependent downregulation of cyclin E-cdk2 activity was associated with increased binding of the cyclin-dependent kinase inhibitor, p21Cip1/WAF1, to the cyclin E-cdk2 complex. Analysis of total cellular p21Cip1/WAF1 showed that in the presence of PF4, p21Cip1/WAF1 levels were sustained at time points when p21Cip1/WAF1 was no longer detectable in cells stimulated by EGF in the absence of PF4. These findings indicate that PF4 inhibition of HUVEC proliferation in response to EGF is associated with impaired downregulation of p21Cip1/WAF1 and provide the first evidence for interference with cell cycle mechanisms by a chemokine.

Selective inhibition of cyclooxygenase (COX)-2 inhibits endothelial cell proliferation by induction of cell cycle arrest

2004 ◽  
Vol 113 (4) ◽  
pp. 541-548 ◽  
Author(s):  
Kentaro Yazawa ◽  
Nelson H. Tsuno ◽  
Joji Kitayama ◽  
Kazushige Kawai ◽  
Yurai Okaji ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Endothelial Cell ◽  
Cell Cycle Arrest ◽  
Selective Inhibition ◽  
Endothelial Cell Proliferation ◽  
Cycle Arrest ◽  
Cox 2
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