scholarly journals Anti-proliferative Effect of Licochalcone A on Vascular Smooth Muscle Cells

2008 ◽  
Vol 31 (11) ◽  
pp. 1996-2000 ◽  
Author(s):  
Jin-Hee Park ◽  
Hyun Joung Lim ◽  
Kuy-Sook Lee ◽  
Seahyoung Lee ◽  
Hyun-Jeong Kwak ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Licochalcone A ◽  
Proliferative Effect

scholarly journals A novel insulin mimetic without a proliferative effect on vascular smooth muscle cells

2000 ◽  
Vol 32 (6) ◽  
pp. 1118-1126 ◽  
Author(s):  
Michael A. Weber ◽  
Anne Lidor ◽  
Subodh Arora ◽  
Gino M. Salituro ◽  
Bei B. Zhang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Insulin Mimetic ◽  
Proliferative Effect

scholarly journals Mechanism of anti-proliferation caused by YC-1, an indazole derivative, in cultured rat A10 vascular smooth-muscle cells

1995 ◽  
Vol 306 (3) ◽  
pp. 787-792 ◽  
Author(s):  
S M Yu ◽  
Z J Cheng ◽  
J H Guh ◽  
F Y Lee ◽  
S C Kuo
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Guanylate Cyclase ◽  
Thymidine Incorporation ◽  
Muscle Cells ◽  
Foetal Calf Serum ◽  
Inhibition Of Proliferation ◽  
Proliferative Effect

An indazole derivative, YC-1, was identified in this study to be capable of reversibly and effectively inhibiting proliferation of rat A10 vascular smooth-muscle cells (VSMCs) in vitro. YC-1 (1-100 microM) dose-dependently inhibited [3H]thymidine incorporation into DNA in rat A10 VSMCs that were synchronized by serum depletion and then restimulated by addition of 10% foetal calf serum (FCS), whereas FCS-induced [3H]thymidine incorporation into rat synchronized endothelial cells was unaffected by this agent. The dose of YC-1 required to cause inhibition of FCS-induced proliferation was similar to that necessary for the formation of cellular cyclic GMP (cGMP). Guanylate cyclase activity in soluble fractions of VSMCs was activated by YC-1 (1-100 microM), whereas cGMP-specific phosphodiesterase activity was unaffected by this compound. The anti-proliferative effect of YC-1 was mimicked by 8-bromo-cGMP, a membrane-permeable cGMP analogue, and was antagonized by KT 5823 (0.2 microM), a selective inhibitor of protein kinase G. The anti-proliferative effect of YC-1 was also antagonized by Methylene Blue (50 microM), a guanylate cyclase inhibitor, and was potentiated by 3-isobutyl-1-methylxanthine (500 microM), a phosphodiesterase inhibitor. These results verified that YC-1 is a direct soluble guanylate cyclase activator in A10 VSMCs, and the anti-proliferative effect of YC-1 is mediated by cGMP. YC-1 still inhibited FCS-induced DNA synthesis even when added 10-18 h after restimulation of the serum-deprived A10 VSMCs with 10% FCS. Flow cytometry in synchronized populations revealed an acute blockage of FCS-inducible cell-cycle progression at a point in the G1/S-phase in YC-1 (100 microM)-treated cells. The inhibition of proliferation by YC-1 was demonstrated to be independent of cell damage, as documented by several criteria of cell viability. In conclusion, YC-1 reversibly and effectively inhibited the proliferation of VSMCs, suggesting that it has potential as a therapeutic agent in the prevention of vascular diseases.

scholarly journals Anti-proliferative effect of prostaglandins A and J on cultured vascular smooth muscle cells

1992 ◽  
Vol 58 ◽  
pp. 288
Author(s):  
Toshiyuki Sasasuri ◽  
Junichi Masuda ◽  
Kentaro Shimokado ◽  
Tasuku Yokota ◽  
Chiva Kosaka ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Proliferative Effect
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