scholarly journals Arginase‐II Induces Vascular Smooth Muscle Cell Senescence and Apoptosis Through p66Shc and p53 Independently of Its l ‐Arginine Ureahydrolase Activity: Implications for Atherosclerotic Plaque Vulnerability

2013 ◽  
Vol 2 (4) ◽  
Author(s):  
Yuyan Xiong ◽  
Yi Yu ◽  
Jean‐Pierre Montani ◽  
Zhihong Yang ◽  
Xiu‐Fen Ming
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Atherosclerotic Plaque ◽  
Cell Senescence ◽  
Plaque Vulnerability ◽  
Arginase Ii

scholarly journals Vascular Smooth Muscle Cell Senescence Promotes Atherosclerosis and Features of Plaque Vulnerability

Circulation ◽  
2015 ◽  
Vol 132 (20) ◽  
pp. 1909-1919 ◽  
Author(s):  
Julie Wang ◽  
Anna K. Uryga ◽  
Johannes Reinhold ◽  
Nichola Figg ◽  
Lauren Baker ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Cell Senescence ◽  
Plaque Vulnerability

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.

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