Deletion of Superoxide Dismutase 1 Blunted Inflammatory Aortic Remodeling in Hypertensive Mice under Angiotensin II Infusion

Superoxide dismutase (SOD) is an enzyme that catalyzes the dismutation of two superoxide anions (O ) into hydrogen peroxide (H O ) and oxygen (O ) and is generally known to protect against oxidative stress. Angiotensin II (AngII) causes vascular hypertrophic remodeling which is associated with H O g...

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Bibliographic Details
Published in:Antioxidants 2021-03, Vol.10 (3), p.471
Main Authors: Shiraishi, Yasunaga, Ishigami, Norio, Kujiraoka, Takehiko, Sato, Atsushi, Fujita, Masanori, Ido, Yasuo, Adachi, Takeshi
Format: Article
Language:English
Subjects:
Angiotensin
Angiotensin II
Anions
Aorta
Blood pressure
Catalase
Coronary vessels
Heparan sulfate
Hydrogen peroxide
Hypertension
Hypertrophy
Inflammation
Interleukin 6
Iodine
Kinases
Oxidation
Oxidative stress
Pathophysiology
Phosphorylation
Polyethylene glycol
siRNA
Smooth muscle
Stat3 protein
Superoxide anions
Superoxide dismutase
superoxide dismutase 1
vascular hypertrophy
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Summary:Superoxide dismutase (SOD) is an enzyme that catalyzes the dismutation of two superoxide anions (O ) into hydrogen peroxide (H O ) and oxygen (O ) and is generally known to protect against oxidative stress. Angiotensin II (AngII) causes vascular hypertrophic remodeling which is associated with H O generation. The aim of this study is to investigate the role of cytosolic SOD (SOD1) in AngII-induced vascular hypertrophy. We employed C57/BL6 mice (WT) and SOD1 deficient mice (SOD1 ) with the same background. They received a continuous infusion of saline or AngII (3.2 mg/kg/day) for seven days. The blood pressures were equally elevated at 1.5 times with AngII, however, vascular hypertrophy was blunted in SOD1 mice compared to WT mice (WT mice 91.9 ± 1.13 µm versus SOD1 mice 68.4 ± 1.41 µm < 0.001). The elevation of aortic interleukin 6 (IL-6) and phosphorylation of pro-inflammatory STAT3 due to AngII were also blunted in SOD1 mice's aortas. In cultured rat vascular smooth muscle cells (VSMCs), reducing expression of SOD1 with siRNA decreased AngII induced IL-6 release as well as phosphorylation of STAT3. Pre-incubation with polyethylene glycol (PEG)-catalase also attenuated phosphorylation of STAT3 due to AngII. These results indicate that SOD1 in VSMCs plays a role in vascular hypertrophy due to increased inflammation caused by AngII, probably via the production of cytosolic H O .
ISSN:2076-3921
2076-3921
DOI:10.3390/antiox10030471