[PP.35.01] ATRAP, A NOVEL INTERACTING MOLECULE WITH AT1 RECEPTOR, INHIBITS ANG II INDUCED PROLIFERATIVE ACTIVITY AND OXIDATIVE STRESS IN RAT SMOOTH MUSCLE CELLS

2016 ◽  
Vol 34 ◽  
pp. e332
Author(s):  
K. Azuma ◽  
K. Tamura ◽  
T. Taira ◽  
H. Wakui ◽  
K. Uneda
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Proliferative Activity ◽  
Muscle Cells ◽  
At1 Receptor ◽  
Ang Ii ◽  
And Oxidative Stress

scholarly journals Epigallocatechin Gallate Attenuates Proliferation and Oxidative Stress in Human Vascular Smooth Muscle Cells Induced by Interleukin-1βvia Heme Oxygenase-1

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Po-Len Liu ◽  
Jung-Tung Liu ◽  
Hsuan-Fu Kuo ◽  
Inn-Wen Chong ◽  
Chong-Chao Hsieh
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Green Tea ◽  
Vascular Smooth Muscle Cells ◽  
Heme Oxygenase ◽  
Muscle Cells ◽  
Heme Oxygenase 1 ◽  
And Oxidative Stress

Proliferation of vascular smooth muscle cells (VSMCs) triggered by inflammatory stimuli and oxidative stress contributes importantly to atherogenesis. The association of green tea consumption with cardiovascular protection has been well documented in epidemiological observations, however, the underlying mechanisms remain unclear. This study aimed to elucidate the effects of the most active green tea catechin derivative, (−)-epigallocatechin-3-gallate (EGCG), in human aortic smooth muscle cells (HASMCs), focusing particularly on the role of a potent anti-inflammatory and antioxidative enzyme heme oxygenase-1 (HO-1). We found that pretreatment of EGCG dose- and time-dependently induced HO-1 protein levels in HASMCs. EGCG inhibited interleukin- (IL-)1β-induced HASMC proliferation and oxidative stress in a dose-dependent manner. The HO-1 inducer CoPPIX decreased IL-1β-induced cell proliferation, whereas the HO-1 enzyme inhibitor ZnPPIX significantly reversed EGCG-caused growth inhibition in IL-1β-treated HASMCs. At the molecular level, EGCG treatment significantly activated nuclear factor erythroid-2-related factor (Nrf2) transcription activities. These results suggest that EGCG might serve as a complementary and alternative medicine in the treatment of these pathologies by inducing HO-1 expression and subsequently decreasing VSMC proliferation.

scholarly journals BCL6 Attenuates Proliferation and Oxidative Stress of Vascular Smooth Muscle Cells in Hypertension

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Dan Chen ◽  
Ying-Hao Zang ◽  
Yun Qiu ◽  
Feng Zhang ◽  
Ai-Dong Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Remodeling ◽  
Ang Ii ◽  
Vsmc Proliferation ◽  
Bcl6 Expression ◽  
And Oxidative Stress

Proliferation and oxidative stress of vascular smooth muscle cells (VSMCs) contribute to vascular remodeling in hypertension and several major vascular diseases. B-cell lymphoma 6 (BCL6) functions as a transcriptional repressor. The present study is designed to determine the roles of BCL6 in VSMC proliferation and oxidative stress and underlying mechanism. Angiotensin (Ang) II was used to induce VSMC proliferation and oxidative stress in human VSMCs. Effects of BCL6 overexpression and knockdown were, respectively, investigated in Ang II-treated human VSMCs. Therapeutical effects of BCL6 overexpression on vascular remodeling, oxidative stress, and proliferation were determined in the aorta of spontaneously hypertensive rats (SHR). Ang II reduced BCL6 expression in human VSMCs. BCL6 overexpression attenuated while BCL6 knockdown enhanced the Ang II-induced upregulation of NADPH oxidase 4 (NOX4), production of reactive oxygen species (ROS), and proliferation of VSMCs. BCL6 expression was downregulated in SHR. BCL6 overexpression in SHR reduced NOX4 expression, ROS production, and proliferation of the aortic media of SHR. Moreover, BCL6 overexpression attenuated vascular remodeling and hypertension in SHR. However, BCL6 overexpression had no significant effects on NOX2 expression in human VSMCs or in SHR. We conclude that BCL6 attenuates proliferation and oxidative stress of VSMCs in hypertension.

Abstract 523: Acetylation of Cyclophilin A in Response to Oxidative Stress Enhances Its Expression and Secretion

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Nwe Nwe Soe ◽  
Mark Sowden ◽  
Bradford C Berk
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Time Dependent ◽  
Dependent Manner ◽  
Ang Ii ◽  
Aortic Smooth Muscle ◽  
Dose Dependent ◽  
Cypa Expression

Objective: Cyclophilin A (CyPA) is a Secreted OXidative stress-induced Factor (SOXF) secreted by cardiovascular cells in response to Angiotensin II (Ang II) and reactive oxygen species (ROS). Extracellular CyPA is a proinflammatory mediator that regulates vascular remodeling, abdominal aortic aneurysm, atherosclerosis and cardiac hypertrophy. Post-translational modification of CyPA by acetylation in response to ROS has been described. Moreover, acetylation of CyPA is important in HIV pathogenesis. The mechanism and regulation of CyPA acetylation as well as its role in cardiovascular diseases are currently unknown. We hypothesized that Ang II regulates oxidative stress-induced CyPA acetylation that alters its expression and/or secretion in vascular smooth muscle cells. Methods and results: Ang II (1μM) increased acetylation of CyPA (Acyl-CyPA) in a time dependent manner, with a peak at 8hr (3.5±0.6 fold increase) in rat aortic smooth muscle cells (RASMC) as shown by Western blot. Mouse aortic smooth muscle cells from mice lacking CyPA (CyPA-/-) and wild type controls (WT) confirmed that Ang II induced acetylation reactivity coincided exactly with CyPA reactivity. In AT1R and CyPA cotransfected HeLa cells, Ang II increased Acyl-CyPA in a time dependent manner consistent with that in RASMC. The ROS scavengers Tiron or N-acetylcysteine significantly inhibited Ang II induced Acyl-CyPA in a dose dependent manner in RASMC. Ang II-induced CyPA acetylation was enhanced by 2 hr pretreatment with histone deacetylase inhibitor trichostatin (TSA) or sirtinol in a dose dependent manner. Similarly, Ang II-induced CyPA secretion was enhanced by pretreatment with TSA (1μM) in a time dependent manner. Moreover, acetyltransferase p300 and PCAF (p300/CBP-asociated factor) inhibitor anacardic acid (6-nonadecyl salicylic acid) dramatically inhibited CyPA expression, and Ang II induced Acyl-CyPA in a dose dependent manner. Conclusion: These results suggest that Ang II-induced CyPA acetylation is oxidative stress dependent, and that acetylation enhanced CyPA expression and secretion. Detailed mechanistic studies of the regulation of CyPA acetylation will help to identify a future therapeutic target for CyPA regulated cardiovascular diseases.

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