Stimulation of endothelial cell proliferation by precursors of thymidylate

1979 ◽  
Vol 100 (1) ◽  
pp. 87-93 ◽  
Author(s):  
B. R. McAuslan ◽  
W. Reilly ◽  
G. N. Hannan
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Endothelial Cell Proliferation ◽  
Stimulation Of

scholarly journals Nitric oxide-dependent stimulation of endothelial cell proliferation by sustained high flow

2008 ◽  
Vol 295 (2) ◽  
pp. H736-H742 ◽  
Author(s):  
Eleni Metaxa ◽  
Hui Meng ◽  
Shashikanth R. Kaluvala ◽  
Michael P. Szymanski ◽  
Rocco A. Paluch ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Proliferation ◽  
Endothelial Cell ◽  
High Flow ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Brdu Incorporation ◽  
Endothelial Cell Proliferation ◽  
Tunel Staining ◽  
No Production ◽  
Stimulation Of

Little is understood about endothelial cell (EC) responses to high flow, which mediate adaptive outward remodeling as well as cerebral aneurysm development. Opposite EC behaviors have been reported in vivo including cell loss during aneurysm initiation and cell proliferation during adaptive outward remodeling. This study aims at elucidating the EC growth response to elevated wall shear stress (WSS) and determining if nitric oxide (NO) is involved. A confluent EC monolayer was subjected to steady-state, laminar flow with WSS ranging from 15 to 100 dyn/cm2 for 24 and 48 h. Cells oriented to the direction of the flow with a time course that varied with WSS. At 48 h, all cells were aligned with the flow. EC proliferation was examined using bromodeoxyuridine (BrdU) incorporation. The percentage of proliferating ECs rose linearly from 15 to 50 dyn/cm2 to more than sixfold at 50–100 dyn/cm2 compared with the accepted physiological baseline of 15–20 dyn/cm2. In addition, terminal deoxynucleotidyl transferase dUTP-mediated nick-end labeling (TUNEL) staining revealed that apoptosis decreased with increasing WSS. These results demonstrate that high WSS stimulates EC proliferation and suppresses apoptosis. Furthermore, immunostaining revealed increased endothelial nitric oxide synthase (eNOS) production with increasing WSS. NOS inhibition with Nω-nitro-l-arginine methyl ester (l-NAME) drastically reduced the WSS-stimulated proliferation, indicating a critical role of NO production in the stimulation of EC proliferation by high WSS.

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