Angiotensin II and IGF-1 Regulate Connexin43 Expression Via ERK and p38 Signaling Pathways in Vascular Smooth Muscle Cells of Coronary Artery Bypass Conduits

2007 ◽  
Vol 142 (1) ◽  
pp. 137-142 ◽  
Author(s):  
Guanghong Jia ◽  
Amit K. Mitra ◽  
Gang Cheng ◽  
Deepak M. Gangahar ◽  
Devendra K. Agrawal
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Signaling Pathways ◽  
Coronary Artery Bypass ◽  
Vascular Smooth Muscle Cells ◽  
Artery Bypass ◽  
Muscle Cells

Different Migration of Vascular Smooth Muscle Cells from Human Coronary Artery Bypass Vessels

2007 ◽  
Vol 44 (2) ◽  
pp. 149-156 ◽  
Author(s):  
Sabine Weiss ◽  
Karin Frischknecht ◽  
Helen Greutert ◽  
Sravan Payeli ◽  
Jan Steffel ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Coronary Artery Bypass ◽  
Vascular Smooth Muscle Cells ◽  
Artery Bypass ◽  
Muscle Cells ◽  
Human Coronary Artery

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
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Receptor Antagonist ◽  
Vascular Smooth Muscle Cells ◽  
Artery Bypass ◽  
Muscle Cells ◽  
Tunel Staining ◽  
Apoptotic Effect

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.

Implication of multiple signaling pathways in the regulation of angiotensin II induced enhanced expression of Giα proteins in vascular smooth muscle cells

2012 ◽  
Vol 90 (8) ◽  
pp. 1105-1116 ◽  
Author(s):  
Yuan Li ◽  
Madhu B. Anand-Srivastava
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Receptor Antagonist ◽  
Signaling Pathways ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Ang Ii ◽  
Enhanced Expression

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.

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