ArticleChinese medical journal2016
Sulfur Dioxide Inhibits Extracellular Signal-regulated Kinase Signaling to Attenuate Vascular Smooth Muscle Cell Proliferation in Angiotensin II-induced Hypertensive Mice.
Article in Chinese medical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Sulfur Dioxide in Food: A Review of Its Preservative Mechanisms, Safety Concerns, and the Rise of Smart Detection Systems.Comprehensive reviews in food science and food safety · 2026Review
- Sulfenylation of ERK1/2: A novel mechanism for SOHeliyon · 2024Article
- Effect of sulfur dioxide on vascular biology.Histology and histopathology · 2021Review
- Endothelial Cell-Derived SOOxidative medicine and cellular longevity · 2021Article
- Sulfur Dioxide Activates ClFrontiers in pharmacology · 2019Article
- Upregulated Expression of Secretory Leukocyte Protease Inhibitor in Lung by Inhalation of High Concentration of Sulfur Dioxide.Chinese medical journal · 2018Article
- Inhibitory Effects of Sulfur Dioxide on Rat Myocardial Fibroblast Proliferation and Migration.Chinese medical journal · 2018Article
- Sulfur dioxide improves endothelial dysfunction by downregulating the angiotensin II/ATJournal of the renin-angiotensin-aldosterone system : JRAASArticle
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8 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundClarifying the mechanisms underlying vascular smooth muscle cell (VSMC) proliferation is important for the prevention and treatment of vascular remodeling and the reverse of hyperplastic lesions. Previous research has shown that the gaseous signaling molecule sulfur dioxide (SO2) inhibits VSMC proliferation, but the mechanism for the inhibition of the angiotensin II (AngII)-induced VSMC proliferation by SO2has not been fully elucidated. This study was designed to investigate if SO2inhibited VSMC proliferation in mice with hypertension induced by AngII.
methodsThirty-six male C57 mice were randomly divided into control, AngII, and AngII + SO2groups. Mice in AngII group and AngII + SO2group received a capsule-type AngII pump implanted under the skin of the back at a slow-release dose of 1000 ng·kg-1·min-1. In addition, mice in AngII + SO2received intraperitoneal injections of SO2donor. Arterial blood pressure of tail artery was determined. The thickness of the aorta was measured by elastic fiber staining, and proliferating cell nuclear antigen (PCNA) and phosphorylated-extracellular signal-regulated kinase (P-ERK) were detected in aortic tissues. The concentration of SO2 in serum and aortic tissue homogenate supernatant was measured using high-performance liquid chromatography with fluorescence determination. In the in vitro study, VSMC of A7R5 cell lines was divided into six groups: control, AngII, AngII + SO2, PD98059 (an inhibitor of ERK phosphorylation), AngII + PD98059, and AngII + SO2 + PD98059. Expression of PCNA, ERK, and P-ERK was determined by Western blotting.
resultsIn animal experiment, compared with the control group, AngII markedly increased blood pressure (P < 0.01) and thickened the aortic wall in mice (P < 0.05) with an increase in the expression of PCNA (P < 0.05). SO2, however, reduced the systemic hypertension and the wall thickness induced by AngII (P < 0.05). It inhibited the increased expression of PCNA and P-ERK induced by AngII (P < 0.05). In cell experiment, PD98059, an ERK phosphorylation inhibitor, blocked the inhibitory effect of SO2on VSMC proliferation (P < 0.05).
conclusionsERK signaling is involved in the mechanisms by which SO2inhibits VSMC proliferation in AngII-induced hypertensive mice via ERK signaling.
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