The Apoptotic Effect of Angiotensin II in Human Vascular Smooth Muscle Cells

2000 ◽  
Vol 6 (S2) ◽  
pp. 636-637
Author(s):  
E. Ou ◽  
C. Wei

Angiotensin II is a potent vasoconstrictor and mitogenic factor. However, the effects of angiotensin II on human vascular smooth muscle cells apoptosis remain controversial. Therefore, the current study was designed to investigate the actions of angiotensin II on human vascular smooth muscle cells apoptosis.Human saphenous vein was obtained from coronary artery bypass surgery (n=6) and was minced and incubated in the special tissue culture system in the absence or presence of angiotensin II (10-6 to 10-12M) for 1, 2, 4, 8, 16, & 24 hours. These studies were repeated with losartan (10-6M, AT- 1 receptor antagonist) and PD-123319 (10-6M, AT-2 receptor antagonist). To detect the DNA fragmentation, in situ terminal deoxymucleotidyl transferase dUTP nick end labeling (TUNEL) and DNA agarose gel analyses were performed. An average of 1000 nuclei was analyzed for TUNEL studies.TUNEL staining and DNA gel analysis demonstrated that angiotensin II increased apoptosis in human vascular smooth muscle cells.

2012 ◽  
Vol 90 (8) ◽  
pp. 1105-1116 ◽  
Author(s):  
Yuan Li ◽  
Madhu B. Anand-Srivastava

We have previously shown that A10 vascular smooth muscle cells (VSMC) exposed to angiotensin II (Ang II) exhibited overexpression of Giα proteins. In the present study, we examined the involvement of different signaling pathways in regulating Ang II induced enhanced expression of Giα proteins in VSMC by using pharmacological inhibitors. Ang II induced increased expression of Giα proteins in A10 VSMC was markedly attenuated by actinomycin D, losartan (an AT1 receptor antagonist), dibutyryl cAMP, phospholipase C (PLC) inhibitor U73122, protein kinase C (PKC) inhibitors staurosporine and GP109203X, but not by PD123319 (an AT2 receptor antagonist). In addition, BAPTA-AM and TMB-8 (chelators of intracellular Ca2+); and nifedipine (a blocker of L-type Ca2+ channels) significantly inhibited Ang II induced enhanced expression of Giα proteins. On the other hand, extracellular Ca2+ chelation using EGTA did not affect the Ang II evoked enhanced levels of Giα proteins. Furthermore, pretreatment of A10 VSMC with calmidazolium (an inhibitor of calmodulin), or KN93 (an inhibitor of CaM kinase), or genistein (an inhibitor of protein tyrosine kinase, PTK), also attenuated the increased levels of Giα proteins induced by Ang II. These results suggest that Ang II induced enhanced expression of Giα proteins may be regulated by different signaling pathways through AT1 receptors in A10 VSMC.


1994 ◽  
Vol 251 (2-3) ◽  
pp. 143-150 ◽  
Author(s):  
Jean-Marc Herbert ◽  
Chantal Delisée ◽  
Frédérique Dol ◽  
Paul Schaeffer ◽  
Catherine Cazaubon ◽  
...  

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