Cigarette smoke-induced oxidative stress activates NRF2 to mediate fibronectin disorganization in vascular formation

Xue, None Jinjiang; Liao, Qiong; Luo, Man; Hua, Chenlei; Zhao, Junwei; Yu, Gangfeng; Chen, Xiangyu; Li, Xueru; Zhang, Xinchun; Ran, None Ruiguo; Lu, Fengying; Wang, Yingxiong; Qiao, Liangjun

doi:10.1098/rsob.210310

Cited by 5 publications

(5 citation statements)

References 48 publications

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“…How Lp(a) can support the development and progression of PAD through intraplaque hemorrhage can only be conjectured. Ex vivo studies show that Lp(a) enhances angiogenesis in the chorioallantoic membrane ( 43 ) and this could synergize with the development of an abnormal angiogenesis observed in smoking ( 44 ) leading to an enhanced plaque development. This pathophysiology might lead to increased bleeding into plaques and contribute to the progress of atherosclerosis in large arteries such as those supplying the lower limbs.…”

Section: Discussionmentioning

confidence: 99%

Epidemiology of atherosclerotic cardiovascular disease in polygenic hypercholesterolemia with or without high lipoprotein(a) levels

Vinci,

Fiotti,

Panizon

et al. 2024

Front. Cardiovasc. Med.

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Background and aimsEpidemiology of atherosclerotic cardiovascular disease might be different in patients with polygenic hypercholesterolemia plus high levels (≥30 mg/dl) of Lp(a) (H-Lpa) than in those with polygenic hypercholesterolemia alone (H-LDL). We compared the incidence of peripheral artery disease (PAD), coronary artery disease (CAD), and cerebrovascular disease (CVD) in patients with H-Lpa and in those with H-LDL.MethodsRetrospective analysis of demographics, risk factors, vascular events, therapy, and lipid profile in outpatient clinical data. Inclusion criteria was adult age, diagnosis of polygenic hypercholesterolemia, and both indication and availability for Lp(a) measurement.ResultsMedical records of 258 patients with H-Lpa and 290 H-LDL were reviewed for occurrence of vascular events. The median duration of follow-up was 10 years (IQR 3–16). In spite of a similar reduction of LDL cholesterol, vascular events occurred more frequently, and approximately 7 years earlier (P = 0.024) in patients with H-Lpa than in H-LDL (HR 1.96 1.21–3.17, P = 0.006). The difference was around 10 years for acute events (TIA, Stroke, acute coronary events) and one year for chronic ones (P = 0.023 and 0.525, respectively). Occurrence of acute CAD was higher in H-Lpa men (HR 3.1, 95% CI 1.2–7.9, P = 0.007) while, among women, PAD was observed exclusively in H-Lpa subjects with smoking habits (P = 0.009).ConclusionsPatients with high Lp(a) levels suffer from a larger and earlier burden of the disease compared to those with polygenic hypercholesterolemia alone. These patients are at higher risk of CAD if they are men, and of PAD if they are women.

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Section: Discussionmentioning

confidence: 99%

Epidemiology of atherosclerotic cardiovascular disease in polygenic hypercholesterolemia with or without high lipoprotein(a) levels

Vinci,

Fiotti,

Panizon

et al. 2024

Front. Cardiovasc. Med.

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“…Research by Xue et al (29) shows that exposure of human umbilical vein endothelial cells (HUVECs) to cigarette extract activates Nrf2 expression. In periodontal disease, increased expression of Nrf2 can prevent periodontal tissue from developing periodontitis and alveolar bone damage, (19) and Li et al (30) showed a decrease in Nrf2 expression in the nucleus and cytoplasm of the diabetic periodontitis group compared with the periodontal tissue control group.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to providing adhesive structural support, which many cell surface receptors recognize, fibronectin also forms a template to which other ECM proteins and soluble growth factors can bind and assemble. (40) Xue et al (29) stated that fibronectin promotes endothelial cell activation, survival, migration, and elongation. Fibronectin interacts with integrins via the RGD (Arg-Gly-Asp) motif to form fibrils, and the complex then binds to focal adhesion kinase (FAK) or actin to carry out various cellular processes.…”

Section: Discussionmentioning

confidence: 99%

Nicotine reduces cell viability and induces oxidative stress in human gingival fibroblasts

Azmi,

Hadi,

Kusuma

et al. 2024

Univ Med

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BackgroundNicotine, as the main component of cigarettes, is known to interfere with the proliferation of human gingival fibroblasts (HGFs) and can trigger oxidative stress. This study aimed to analyze the impact of nicotine on viability, expression of the antioxidant Nrf2, levels of the product of oxidative stress malondialdehyde (MDA), and the migration capacity of HGFs. MethodsAn experimental laboratory study used fibroblasts isolated from healthy human gingiva. The cells were grouped into the non-treatment control group (NTC), the solvent control (SC), and the treatment groups, exposed to nicotine at various concentrations for twenty-four hours. Cell viability was assesed using the cell counting kit-8 (CCK-8), Nrf2 expression was examined using ELISA, MDA level was measured using an MDA kit, and migration capacity was assessed using a scratch assay. Statistical analysis used one-way Anova or Kruskal-Wallis test. A p-value of <0.05 was expressed statistically significant. ResultsThe Cell viability was substantially reduced in the nicotine group compared to the untreated group, accompanied by changes in cell morphology. In contrast, Nrf2 expression increased significantly (p=0.010) in the 5 mM nicotine group compared with the control group. The MDA levels were not significantly distinct across groups (p=0.056). Cell migration was delayed significantly in the 5 mM nicotine group at 72 hours after scratching compared to the control group. ConclusionNicotine decreased HGFs viability and increased Nrf2 expression significantly in a dose-dependent manner. Nicotine at 5 mM concentration did not alter MDA levels but delayed cell migration.

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“…Cigarette smoke has been reported to increase the oxidative stress leading to the dysregulation of reactive oxygen species production as the marker of oxidative stress. 18 Due to the imbalance in the generation and scavenging of ROS, the ROS accumulates leading to tissue damage. 19 Quinine has been reported to be involved in the electron transport chain and decreasing its activity.…”

Section: Discussionmentioning

confidence: 99%

Quinine Attenuates Cigarette Smoke Extract Induced Mucosal Inflammation and Oxidative Stress in the Zebrafish Model

Alqasmi¹

2023

Ind. J. Pharm. Edu. Res.

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Introduction: Smoking is the primary cause of Chronic obstructive pulmonary disease (COPD) leading to alarming increase in worldwide death. Cigarette smoking is a dangerous risk factor in causing mucosal inflammation and lung damage caused by nicotine, which is more addictive than other narcotics. This study was undertaken to assess the potential of quinine in ameliorating the cigarette smoke extract (CSE) induced inflammation in the Zebrafish model. Materials and Methods: CSE was extracted in water and the Zebrafish was exposed to concentrations ranging from 0.2 to 1.0 cig/L. IC 50 of CSE was found to be 0.3 cig/L and this concentration was used for further studies. Induced Zebrafish were treated with 5 mg, 10mg and 15 mg/kg of quinine and analysed for reactive oxygen species, nitric oxide levels, myeloperoxidase activity, histopathology and expression of pro-inflammatory (IL-1) and anti-inflammatory (IL-10) cytokine. Results: The results indicate that exposure of Zebrafish to CSE has significantly increased the levels of ROS, MPO, NO and pro-inflammatory cytokine. Upon treatment with quinine, a dose dependent decrease in these levels was observed with the significantly higher decrease in 15mg/kg treated animals for 8 days. The levels of the anti-inflammatory cytokine, IL-10 tend to be increased with increasing concentration of quinine. The histopathological examination has shown inflammation and damaged gill filaments in the CSE exposed group the Gills inflammation and damaged gill filaments with increased neutrophil accumulation whereas these changes are not observed in the quinine-treated animals. Conclusion: Cumulatively, the results obtained in this study confirm the role of quinine in ameliorating the CSE-induced inflammation in the Zebrafish model.

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Cigarette smoke-induced oxidative stress activates NRF2 to mediate fibronectin disorganization in vascular formation

Cited by 5 publications

References 48 publications

Epidemiology of atherosclerotic cardiovascular disease in polygenic hypercholesterolemia with or without high lipoprotein(a) levels

Epidemiology of atherosclerotic cardiovascular disease in polygenic hypercholesterolemia with or without high lipoprotein(a) levels

Nicotine reduces cell viability and induces oxidative stress in human gingival fibroblasts

Quinine Attenuates Cigarette Smoke Extract Induced Mucosal Inflammation and Oxidative Stress in the Zebrafish Model

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