scholarly journals Mitochondrial Morphofunctional Alterations in Smooth Muscle Cells of Aorta in Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
María del Carmen Baez ◽  
Mariana Tarán ◽  
Candelaria Llorens ◽  
Ariel Balceda ◽  
María de La Paz Scribano ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vitamin E ◽  
Smooth Muscle Cells ◽  
Experimental Model ◽  
Citrate Synthase ◽  
Muscle Cells ◽  
Male Rats ◽  
Aortic Smooth Muscle ◽  
Mitochondrial Alterations ◽  
And Oxidative Stress

In an experimental model of atherogenesis induced by hyperfibrinogenemia (HF), the pharmacological response of vitamin E was studied in order to assess its antioxidant effect on the mitochondrial morphofunctional alterations in aortic smooth muscle cells. Three groups of male rats were used: (Ctr) control, (AI) atherogenesis induced for 120 days, and (AIE) atherogenesis induced for 120 days and treated with vitamin E. HF was induced by adrenalin injection (0.1 mg/day/rat) for 120 days. AIE group was treated with the administration of 3.42 mg/day/rat of vitamin E for 105 days after the first induction. Mitochondria morphology was analyzed by electronic microscopy (EM) and mitochondrial complexes (MC) by spectrophotometry. In group AI the total and mean number of mitochondria reduced significantly, the intermembranous matrix increased, and swelling was observed with respect to Ctr and AIE (P<0.01). These damages were related to a significant decrease in the activity of citrate synthase and complexes I, II, III, and IV in group AI in comparison to Ctr (P<0.001). Similar behavior was presented by group AI compared to AIE (P<0.001). These results show that vitamin E produces a significative regression of inflammatory and oxidative stress process and it resolved the morphofunctional mitochondrial alterations in this experimental model of atherogenic disease.

Changes of Superoxide Dismutase in Cultured Rat Aortic Smooth Muscle Cells (A7r5) by an Incubation of Vitamin E

Pharmacology ◽  
1999 ◽  
Vol 59 (5) ◽  
pp. 275-282 ◽  
Author(s):  
Wen-Pin Huang ◽  
Paul Chan ◽  
Yi-Jen Chen ◽  
Chi-Ming Chen ◽  
Shue-Sen Liao ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Smooth Muscle ◽  
Vitamin E ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle

scholarly journals Abnormal Ribosome Biogenesis Partly Induced p53-Dependent Aortic Medial Smooth Muscle Cell Apoptosis and Oxidative Stress

2019 ◽  
Vol 2019 ◽  
pp. 1-19
Author(s):  
Qi Wu ◽  
Junmou Hong ◽  
Zhiwei Wang ◽  
Junxia Hu ◽  
Ruoshi Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Ribosome Biogenesis ◽  
Muscle Cells ◽  
Synthesis Rate ◽  
Protein Synthesis Rate ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
And Oxidative Stress

Ribosome biogenesis is a crucial biological process related to cell proliferation, redox balance, and muscle contractility. Aortic smooth muscle cells (ASMCs) show inhibition of proliferation and apoptosis, along with high levels of oxidative stress in aortic dissection (AD). Theoretically, ribosome biogenesis should be enhanced in the ASMCs at its proliferative state but suppressed during apoptosis and oxidative stress. However, the exact status and role of ribosome biogenesis in AD are unknown. We therefore analyzed the expression levels of BOP1, a component of the PeBoW complex which is crucial to ribosome biogenesis, in AD patients and a murine AD model and its influence on the ASMCs. BOP1 was downregulated in the aortic tissues of AD patients compared to healthy donors. In addition, overexpression of BOP1 in human aortic smooth muscle cells (HASMCs) inhibited apoptosis and accumulation of p53 under hypoxic conditions, while knockdown of BOP1 decreased the protein synthesis rate and motility of HASMCs. The RNA polymerase I inhibitor cx-5461 induced apoptosis, ROS production, and proliferative inhibition in the HASMCs, which was partly attenuated by p53 knockout. Furthermore, cx-5461 aggravated the severity of AD in vivo, but a p53-/- background extended the life-span and lowered AD incidence in the mice. Taken together, decreased ribosome biogenesis in ASMCs resulting in p53-dependent proliferative inhibition, oxidative stress, and apoptosis is one of the underlying mechanisms of AD.

Effect of vitamin E and allylamine on the proliferation of cultured aortic smooth muscle cells from streptozotocin-induced diabetic rats

Life Sciences ◽  
1999 ◽  
Vol 64 (25) ◽  
pp. 2317-2325 ◽  
Author(s):  
Hiromitsu Sasaki ◽  
Jiro Nakamura ◽  
Naoki Koh ◽  
Yoji Hamada ◽  
Tomohiro Hara ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vitamin E ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Diabetic Rats ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle

Sorghum Fermented by Aspergillus oryzae NK Enhances Inhibition of Vascular Inflammation in TNF-α-stimulated Human Aortic Smooth Muscle Cells

2018 ◽  
Vol 88 (5-6) ◽  
pp. 309-318
Author(s):  
Hae Seong Song ◽  
Jung-Eun Kwon ◽  
Hyun Jin Baek ◽  
Chang Won Kim ◽  
Hyelin Jeon ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Inflammatory Response ◽  
Smooth Muscle Cells ◽  
Adhesion Molecule ◽  
Vascular Inflammation ◽  
Muscle Cells ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Tnf Α ◽  
Cox 2

Abstract. Sorghum bicolor L. Moench is widely grown all over the world for food and feed. The effects of sorghum extracts on general inflammation have been previously studied, but its anti-vascular inflammatory effects are unknown. Therefore, this study investigated the anti-vascular inflammation effects of sorghum extract (SBE) and fermented extract of sorghum (fSBE) on human aortic smooth muscle cells (HASMCs). After the cytotoxicity test of the sorghum extract, a series of experiments were conducted. The inhibition effects of SBE and fSBE on the inflammatory response and adhesion molecule expression were measured using treatment with tumor necrosis factor-α (TNF-α), a crucial promoter for the development of atherosclerotic lesions, on HASMCs. After TNF-α (10 ng/mL) treatment for 2 h, then SBE and fSBE (100 and 200 μg/mL) were applied for 12h. Western blotting analysis showed that the expression of vascular cell adhesion molecule-1 (VCAM-1) (2.4-fold) and cyclooxygenase-2 (COX-2) (6.7-fold) decreased, and heme oxygenase-1 (HO-1) (3.5-fold) increased compared to the TNF-α control when treated with 200 μg/mL fSBE (P<0.05). In addition, the fSBE significantly increased the expression of HO-1 and significantly decreased the expression of VCAM-1 and COX-2 compared to the TNF-α control in mRNA level (P<0.05). These reasons of results might be due to the increased concentrations of procyanidin B1 (about 6-fold) and C1 (about 30-fold) produced through fermentation with Aspergillus oryzae NK for 48 h, at 37 °C. Overall, the results demonstrated that fSBE enhanced the inhibition of the inflammatory response and adherent molecule expression in HASMCs.

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