Hyperinsulinemia-induced vascular smooth muscle cell (VSMC) migration and proliferation is mediated by converging mechanisms of mitochondrial dysfunction and oxidative stress

2012 ◽  
Vol 373 (1-2) ◽  
pp. 95-105 ◽  
Author(s):  
Shiny Abhijit ◽  
Regin Bhaskaran ◽  
Abirami Narayanasamy ◽  
Anand Chakroborty ◽  
Nagaraj Manickam ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Mitochondrial Dysfunction ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
And Oxidative Stress

Uric acid stimulates vascular smooth muscle cell proliferation and oxidative stress via the vascular renin–angiotensin system

2008 ◽  
Vol 26 (2) ◽  
pp. 269-275 ◽  
Author(s):  
Dalila B Corry ◽  
Pirooz Eslami ◽  
Kei Yamamoto ◽  
Michael D Nyby ◽  
Hirofumi Makino ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Proliferation ◽  
Uric Acid ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
And Oxidative Stress

Abstract 372: Role of Redox-Sensitive Calcium Channel TRPM2 and Oxidative Stress in Vascular Smooth Muscle Cell Differentiation to an Osteogenic Phenotype: Implications in Hypertension.

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Augusto C Montezano ◽  
Hiba Yusuf ◽  
Glaucia E Callera ◽  
Rhian M Touyz
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Molecular Mechanisms ◽  
Ros Generation ◽  
Phenotype Transition ◽  
And Oxidative Stress

Vascular smooth muscle cell (VSMC) transformation to an osteoblast-like phenotype is a major factor contributing to vascular calcification, often associated with chronic kidney disease and hypertension. Exact molecular mechanisms underlying VSMC transformation remain unclear but intracellular calcium and ROS have been implicated. Whether these factors are interlinked is unknown. Here, we tested the hypothesis that ROS and redox-sensitive calcium channels (TRPM2) induce an osteogenic phenotype transition in VSMCs from WKY and SHRSP rats. Cultured VSMCs from WKY and SHRSP rats were exposed to calcification medium (CaM) (Ca2+ 1.8 mmol/L, PO4 2.0 mmol/L) for 10 days in the presence/absence of tempol (superoxide dismutase mimetic), and N-(p-amylcinnamoyl)anthranilic acid (ACA, TRPM2 inhibitor). Osteocalcin (OC), BMP-2, BMP-7, TRPM2 and TRPM2-S expression, as well as p47 phox translocation (cytosol:membrane), were determined by immunoblotting. ROS generation was evaluated by chemioluminescence. ROS production (Ctl: 30 AU/ug protein; CaM: 60 AU/ug protein, p<0.05) and p47 translocation (Ctl: 0.7 AU; CaM: 1.1AU, p<0.05) were increased by the CaM in VSMCs from WKY. CaM-induced increase in OC (Ctl: 5 AU; CaM: 13 AU) and BMP-2 (Ctl: 0.60 AU; CaM: 0.75AU) (p<0.05), followed by a decrease in BMP-7 (Ctl: 1.12 AU; CaM: 0.7 AU) (p<0.05), expression in VSMCs from WKY; an effect that was inhibited by tempol and ACA. In SHRSP, the increase in OC (Ctl: 1.25 AU; CaM: 2 AU) and BMP-2 (Ctl: 0.6 AU; CaM: 0.85 AU, p<0.05) expression induced by the CaM was also blocked by tempol. TRPM2 expression was higher in SHRSP (1.40 AU) than in WKY (1.05 AU) VSMCs (p<0.05). However, TRPM2-S expression, an intracellular inhibitor of TRPM2, was decreased in SHRSP compared to WKY VSMCs (SHRSP: 0.9 AU; WKY: 1.5 AU; p<0.05), and it was further decreased by the CaM (0.6 AU). In conclusion, ROS, through TRPM-2 sensitive mechanisms, seems to play an important role in VSMC transformation to an osteogenic, a phenomenon that may be exacerbated in hypertension.

Renin and (pro)renin receptor induced vascular smooth muscle cell proliferation and neointimal hyperplasia by activating oxidative stress and inflammation

2021 ◽  
Author(s):  
Nana Zhang ◽  
Xiaosu Song ◽  
Yunfei Bian ◽  
Rui Bai ◽  
Huiyu Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Proliferation ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Neointimal Hyperplasia ◽  
Akt Pathway

Abstract Background Numerous studies have shown that the proliferation and migration of vascular smooth muscle cells (VSMCs) were the pathological basis of restenosis occurrence. And Renin and prorenin could promote the proliferation of VSMCs through (pro)renin receptor ((P)RR). Therefore, this study aimed to observe the role of (P)RR in the proliferation of VSMCs in vitro and neointimal hyperplasia in the arterial injury model. Methods Cell proliferation was measured by CCK-8 and flow cytometry; RT-PCR and WB assays were used to detect the expressions of cyclin D1, PCNA, (P)RR, NOX1, and PI3K/AKT signal proteins; immunofluorescent staining was conducted to measure the expression of (P)RR; the levels of renin, PDGF-BB, inflammatory factors, and oxidative stress were determined by ELISA; pathological change was observed by HE staining. Results In this study, we demonstrated that renin could promote the proliferation of rat VSMCs by enhanced cell viability and cell cycle proteins, but silencing (P)RR restrained this. Then, we found that renin could enhance the levels of NOX1-mediated oxidative stress and inflammation by activating ERK1/2-AKT pathway in vitro. Similarly, inhibition of (P)RR resulted in opposite phenomenon. Importantly, inhibition of (P)RR could inhibit the neointimal hyperplasia in vivo after common carotid artery injury through restraining NOX1-mediated oxidative stress by down-regulating ERK1/2-AKT pathway. Conclusion We concluded that renin and (P)RR induced vascular smooth muscle cell proliferation and neointimal hyperplasia by activating oxidative stress, inflammation and ERK1/2-AKT pathway in an angiotensin Ⅱ (Ang Ⅱ)-independent manner.

scholarly journals Wnt5a-Induced Wnt1-Inducible Secreted Protein-1 Suppresses Vascular Smooth Muscle Cell Apoptosis Induced by Oxidative Stress

2014 ◽  
Vol 34 (11) ◽  
pp. 2449-2456 ◽  
Author(s):  
Carina Mill ◽  
Bethan Alice Monk ◽  
Helen Williams ◽  
Steven John Simmonds ◽  
Jamie Yancey Jeremy ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Cell Apoptosis ◽  
Secreted Protein ◽  
Muscle Cell Apoptosis
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