Enhanced expression of Gqα and PLC-β1 proteins contributes to vascular smooth muscle cell hypertrophy in SHR: role of endogenous angiotensin II and endothelin-1

2014 ◽  
Vol 307 (1) ◽  
pp. C97-C106 ◽  
Author(s):  
Mohammed Emehdi Atef ◽  
Madhu B. Anand-Srivastava
Keyword(s):  
Protein Synthesis ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Ang Ii ◽  
Enhanced Expression

Vascular Gqα signaling has been shown to contribute to cardiac hypertrophy. In addition, angiotensin II (ANG II) was shown to induce vascular smooth muscle cell (VSMC) hypertrophy through Gqα signaling; however, the studies on the role of Gqα and PLC-β1 proteins in VSMC hypertrophy in animal model are lacking. The present study was therefore undertaken to examine the role of Gqα/PLC-β1 proteins and the signaling pathways in VSMC hypertrophy using spontaneously hypertensive rats (SHR). VSMC from 16-wk-old SHR and not from 12-wk-old SHR exhibited enhanced levels of Gqα/PLC-β1 proteins compared with age-matched Wistar-Kyoto (WKY) rats as determined by Western blotting. However, protein synthesis as determined by [3H]leucine incorporation was significantly enhanced in VSMC from both 12- and 16-wk-old SHR compared with VSMC from age-matched WKY rats. Furthermore, the knockdown of Gqα/PLC-β1 in VSMC from 16-wk-old SHR by antisense and small interfering RNA resulted in attenuation of protein synthesis. In addition, the enhanced expression of Gqα/PLC-β1 proteins, enhanced phosphorylation of ERK1/2, and enhanced protein synthesis in VSMC from SHR were attenuated by the ANG II AT1 and endothelin-1 (ET-1) ETA receptor antagonists losartan and BQ123, respectively, but not by the ETB receptor antagonist BQ788. In addition, PD98059 decreased the enhanced expression of Gqα/PLC-β1 and protein synthesis in VSMC from SHR. These results suggest that the enhanced levels of endogenous ANG II and ET-1 through the activation of AT1 and ETA receptors, respectively, and MAP kinase signaling, enhanced the expression of Gqα/PLC-β1 proteins in VSMC from 16-wk-old SHR and result in VSMC hypertrophy.

scholarly journals Protective role of vascular smooth muscle cell PPARγ in angiotensin II-induced vascular disease

2012 ◽  
Vol 97 (3) ◽  
pp. 562-570 ◽  
Author(s):  
Chiara Marchesi ◽  
Asia Rehman ◽  
Yohann Rautureau ◽  
Daniel A. Kasal ◽  
Marie Briet ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Vascular Disease ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Protective Role

Angiotensin II and Amyloid-β Synergistically Induce Brain Vascular Smooth Muscle Cell Senescence

2020 ◽  
Author(s):  
Hui-Yu Bai ◽  
Li-Juan Min ◽  
Bao-Shuai Shan ◽  
Jun Iwanami ◽  
Harumi Kan-no ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Amyloid Β ◽  
Cell Senescence ◽  
Ang Ii ◽  
Dose Combination

Abstract Background Amyloid-β (Aβ) induces cerebrovascular damage and is reported to stimulate endothelial cell senescence. We previously demonstrated that angiotensin II (Ang II) promoted vascular senescence. We examined the possible cross-talk between Ang II and Aβ in regulating brain vascular smooth muscle cell (BVSMC) senescence. Methods BVSMC were prepared from adult male mice and stimulated with Ang II (0, 0.1, 1, 10, 100 nmol/L) and/or Aβ 1-40 (0, 0.1, 0.3, 0.5, 1, 3, 5 µmol/L) for the indicated times. Cellular senescence was evaluated by senescence-associated β-galactosidase staining. Results Treatment with Ang II (100 nmol/L) or Aβ (1 µmol/L) at a higher dose increased senescent cells compared with control at 6 days. Treatment with Ang II (10 nmol/L) or Aβ (0.5 µmol/L) at a lower dose had no effect on senescence whereas a combined treatment with lower doses of Ang II and Aβ significantly enhanced senescent cells. This senescence enhanced by lower dose combination was markedly blocked by valsartan (Ang II type 1 receptor inhibitor) or TAK-242 (Aβ receptor TLR4 inhibitor) treatment. Moreover, lower dose combination caused increases in superoxide anion levels and p-ERK expression for 2 days, NF-κB activity, p-IκB, p-IKKα/β, p16 and p53 expression for 4 days, and an obvious decrease in pRb expression. These changes by lower dose combination, except in p-IκB expression and NF-κB activity, were significantly inhibited by pretreatment with U0126 (ERK inhibitor). Conclusions Ang II and Aβ synergistically promoted BVSMC senescence at least due to enhancement of the p-ERK-p16-pRb signaling pathway, oxidative stress and NF-κB/IκB activity.

Soluble klotho attenuates angiotensin II-mediated vascular smooth muscle cell ageing: role of Nrf2-antioxidant signalling

2016 ◽  
Vol 96 ◽  
pp. S25
Author(s):  
Giuseppe Maltese ◽  
Paraskevi-Maria Psefteli ◽  
Salil Srivastava ◽  
Benedetta Rizzo ◽  
Luigi Gnudi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell

scholarly journals Angiotensin II Type 2 Receptor Mediates Vascular Smooth Muscle Cell Apoptosis in Cystic Medial Degeneration Associated With Marfan’s Syndrome

Circulation ◽  
2001 ◽  
Vol 104 (suppl_1) ◽  
Author(s):  
Hirotaka Nagashima ◽  
Yasunari Sakomura ◽  
Yoshikazu Aoka ◽  
Kenta Uto ◽  
Kin-ichi Kameyama ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Ace Inhibitor ◽  
Ang Ii ◽  
Medial Degeneration

Background Cystic medial degeneration (CMD) is a histological abnormality that is common in the aortic diseases associated with Marfan’s syndrome (MFS). Although little known about the mechanism underlying CMD, several recent reports have demonstrated that vascular smooth muscle cell (VSMC) apoptosis could play a substantial role in CMD. On the other hand, angiotensin II (Ang II) has been reported to play an important role in the regulation of VSMC growth and apoptosis via the Ang II type 1 receptor (AT1R) and type 2 receptor (AT2R). Methods and Results To elucidate the role of Ang II signaling via the Ang II receptors in CMD, we investigated AT1R and AT2R mRNA expression and tissue concentration of Ang II in MFS aortas (n=10) and control aortas (n=12). Furthermore, we examined the effects of an ACE inhibitor, an AT1R blocker, and an AT2R blocker on serum deprivation-induced VSMC apoptosis by organ culture system. AT1R expression was significantly decreased ( P <0.01) and AT2R expression was significantly increased ( P <0.001) in MFS aortas compared with control aortas, and tissue Ang II concentration was significantly higher in CMD than in the control condition ( P <0.01). Both the ACE inhibitor and AT2R blocker significantly inhibited serum deprivation-induced VSMC apoptosis ( P <0.05), although the AT1R blocker did not inhibit apoptosis in cultured aortic media from MFS patients. Conclusions Accelerated ACE-dependent Ang II formation and signaling via upregulated AT2R play a pivotal role in VSMC apoptosis in CMD, and the ACE inhibitor could have clinical value in the prevention and treatment of CMD.

The role of the endothelium in the regulation of vascular smooth muscle cell contractions induced by angiotensin II after ischemia and reperfusion

2010 ◽  
Vol 33 (7) ◽  
pp. 1019-1024 ◽  
Author(s):  
Katarzyna Szadujkis-Szadurska ◽  
Maciej Slupski ◽  
Rafal Szadujkis-Szadurski ◽  
Leszek Szadujkis-Szadurski ◽  
Milosz Jasiñski ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Ischemia And Reperfusion
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