scholarly journals Effects of mild steel welding fume particles on pulmonary epithelial inflammation and endothelial activation

2020 ◽  
Vol 36 (12) ◽  
pp. 995-1001
Author(s):  
Johanna Samulin Erdem ◽  
Yke Jildouw Arnoldussen ◽  
Sepideh Tajik ◽  
Dag G Ellingsen ◽  
Shanbeh Zienolddiny
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Mild Steel ◽  
Endothelial Activation ◽  
Repeated Exposure ◽  
Welding Fume ◽  
Inflammatory Status ◽  
Increased Risk ◽  
And Migration ◽  
Mild Steel Welding

Welders have an increased risk for cardiovascular disease (CVD) following exposure to welding fumes. The underlying mechanisms are largely unknown; however, oxidative stress, systemic inflammation, and endothelial dysfunction have been suggested as contributing factors to particle-induced CVD. We investigated effects of mild steel welding fume (MSWF) on three target cell types: macrophages, pulmonary epithelial, and vascular endothelial cells. Cells were exposed to MSWF at nontoxic doses for 6 h/day, for five consecutive days. The expression of 40 genes involved in inflammation, fibrosis, and endothelial activation was analyzed. Moreover, changes in the reactive oxygen species production and migration capacity of cells were assessed. The expression of matrix metallopeptidase 1 ( MMP1) was induced in both epithelial and endothelial cells following repeated exposure to MSWF. Although MMP1 is important in inflammatory responses in vivo, this effect was not concurrent with changes in the inflammatory status, cell proliferation, and migration capacities, nor did it induce oxidative stress in the cells. Thus, repeated exposure with low doses of MSWF was sufficient neither for inducing inflammatory stress in epithelial cells and macrophages nor for endothelial activation, and higher concentrations of MSWF or the nonparticle fraction of MSWF may be critical in causing the increased risk of CVD observed among welders.

scholarly journals Chronic Benzene Exposure Aggravates Pressure Overload-Induced Cardiac Dysfunction

2021 ◽  
Author(s):  
Igor N Zelko ◽  
Sujith Dassanayaka ◽  
Marina V Malovichko ◽  
Caitlin M Howard ◽  
Lauren F Garrett ◽  
...  
Keyword(s):  
Heart Failure ◽  
Endothelial Cells ◽  
Cardiac Function ◽  
Cardiac Tissue ◽  
Pressure Overload ◽  
Endothelial Activation ◽  
Air Exposure ◽  
Benzene Exposure ◽  
Increased Risk

Benzene is a ubiquitous environmental pollutant abundant in household products, petrochemicals and cigarette smoke. Benzene is a well-known carcinogen in humans and experimental animals; however, little is known about the cardiovascular toxicity of benzene. Recent population-based studies indicate that benzene exposure is associated with an increased risk for heart failure. Nonetheless, it is unclear whether benzene exposure is sufficient to induce and/or exacerbate heart failure. We examined the effects of benzene (50 ppm, 6 h/day, 5 days/week, 6 weeks) or HEPA-filtered air exposure on transverse aortic constriction (TAC)-induced pressure overload in male C57BL/6J mice. Our data show that benzene exposure had no effect on cardiac function in the Sham group; however, it significantly compromised cardiac function as depicted by a significant decrease in fractional shortening and ejection fraction, as compared with TAC/Air-exposed mice. RNA-seq analysis of the cardiac tissue from the TAC/benzene-exposed mice showed a significant increase in several genes associated with adhesion molecules, cell-cell adhesion, inflammation, and stress response. In particular, neutrophils were implicated in our unbiased analyses. Indeed, immunofluorescence studies showed that TAC/benzene exposure promotes infiltration of CD11b+/S100A8+/myeloperoxidase+-positive neutrophils in the hearts by 3-fold. In vitro, the benzene metabolites, hydroquinone and catechol, induced the expression of P-selectin in cardiac microvascular endothelial cells by 5-fold and increased the adhesion of neutrophils to these endothelial cells by 1.5-2.0-fold. Benzene metabolite-induced adhesion of neutrophils to the endothelial cells was attenuated by anti-P-selectin antibody. Together, these data suggest that benzene exacerbates heart failure by promoting endothelial activation and neutrophil recruitment.

scholarly journals Blood-derived extracellular vesicles isolated from healthy donors exposed to air pollution modulate in vitro endothelial cells behavior

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Federica Rota ◽  
Luca Ferrari ◽  
Mirjam Hoxha ◽  
Chiara Favero ◽  
Rita Antonioli ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Extracellular Vesicles ◽  
Positive Association ◽  
Endothelial Activation ◽  
Normal Weight ◽  
Markers Of Inflammation ◽  
Healthy Donors ◽  
Increased Risk ◽  
Peripheral Cells

AbstractThe release of Extracellular Vesicles (EVs) into the bloodstream is positively associated with Particulate Matter (PM) exposure, which is involved in endothelial dysfunction and related to increased risk of cardiovascular disease. Obesity modifies the effects of PM exposure on heart rate variability and markers of inflammation, oxidative stress, and acute phase response. We isolated and characterized plasmatic EVs from six healthy donors and confirmed a positive association with PM exposure. We stratified for Body Mass Index (BMI) and observed an increased release of CD61+ (platelets) and CD105+ (endothelium) derived-EVs after high PM level exposure in Normal Weight subjects (NW) and no significant variations in Overweight subjects (OW). We then investigated the ability to activate endothelial primary cells by plasmatic EVs after both high and low PM exposure. NW-high-PM EVs showed an increased endothelial activation, measured as CD105+/CD62e+ (activated endothelium) EVs ratio. On the contrary, cells treated with OW-high-PM EVs showed reduced endothelial activation. These results suggest the ability of NW plasmatic EVs to communicate to endothelial cells and promote the crosstalk between activated endothelium and peripheral cells. However, this capacity was lost in OW subjects. Our findings contribute to elucidate the role of EVs in endothelial activation after PM exposure.

Persistence of deposited metals in the lungs after stainless steel and mild steel welding fume inhalation in rats

2010 ◽  
Vol 85 (5) ◽  
pp. 487-498 ◽  
Author(s):  
James M. Antonini ◽  
Jenny R. Roberts ◽  
Samuel Stone ◽  
Bean T. Chen ◽  
Diane Schwegler-Berry ◽  
...  
Keyword(s):  
Stainless Steel ◽  
Mild Steel ◽  
Welding Fume ◽  
Mild Steel Welding

scholarly journals Differential Responses to Bioink-Induced Oxidative Stress in Endothelial Cells and Fibroblasts

2021 ◽  
Vol 22 (5) ◽  
pp. 2358
Author(s):  
Hatice Genç ◽  
Jonas Hazur ◽  
Emine Karakaya ◽  
Barbara Dietel ◽  
Faina Bider ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Cell Viability ◽  
Human Fibroblasts ◽  
Ros Generation ◽  
Cytotoxic Effects ◽  
Thiol Content ◽  
And Migration ◽  
Aldehyde Groups ◽  
The Relationship

A hydrogel system based on oxidized alginate covalently crosslinked with gelatin (ADA-GEL) has been utilized for different biofabrication approaches to design constructs, in which cell growth, proliferation and migration have been observed. However, cell–bioink interactions are not completely understood and the potential effects of free aldehyde groups on the living cells have not been investigated. In this study, alginate, ADA and ADA-GEL were characterized via FTIR and NMR, and their effect on cell viability was investigated. In the tested cell lines, there was a concentration-dependent effect of oxidation degree on cell viability, with the strongest cytotoxicity observed after 72 h of culture. Subsequently, primary human cells, namely fibroblasts and endothelial cells (ECs) were grown in ADA and ADA-GEL hydrogels to investigate the molecular effects of oxidized material. In ADA, an extremely strong ROS generation resulting in a rapid depletion of cellular thiols was observed in ECs, leading to rapid necrotic cell death. In contrast, less pronounced cytotoxic effects of ADA were noted on human fibroblasts. Human fibroblasts had higher cellular thiol content than primary ECs and entered apoptosis under strong oxidative stress. The presence of gelatin in the hydrogel improved the primary cell survival, likely by reducing the oxidative stress via binding to the CHO groups. Consequently, ADA-GEL was better tolerated than ADA alone. Fibroblasts were able to survive the oxidative stress in ADA-GEL and re-entered the proliferative phase. To the best of our knowledge, this is the first report that shows in detail the relationship between oxidative stress-induced intracellular processes and alginate di-aldehyde-based bioinks.

scholarly journals ABCG1 Attenuates Oxidative Stress Induced by H2O2 through the Inhibition of NADPH Oxidase and the Upregulation of Nrf2-Mediated Antioxidant Defense in Endothelial Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Jiahong Xue ◽  
Jiali Fan ◽  
Yuan Li ◽  
Wenhuan Wu ◽  
Qing Yan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Nadph Oxidase ◽  
Oxidase Activity ◽  
Antioxidant Defense ◽  
Endothelial Activation ◽  
Nadph Oxidase Activity ◽  
Protein Levels ◽  
Mda Content ◽  
Intracellular Cholesterol

Summary. Oxidative stress is an important factor that is related to endothelial dysfunction. ATP-binding cassette transporter G1 (ABCG1), a regulator of intracellular cholesterol efflux, has been found to prevent endothelial activation in vessel walls. To explore the role of ABCG1 in oxidative stress production in endothelial cells, HUAECs were exposed to H2O2 and transfected with the specific ABCG1 siRNA or ABCG1 overexpression plasmid. The results showed that overexpression of ABCG1 by ABCG1 plasmid or liver X receptor (LXR) agonist T0901317 treatment inhibited ROS production and MDA content induced by H2O2 in HUAECs. Furthermore, ABCG1 upregulation blunted the activity of prooxidant NADPH oxidase and the expression of Nox4, one of the NADPH oxidase subunits. Moreover, the increased migration of Nrf2 from the cytoplasm to the nucleus and antioxidant HO-1 expression were detected in HUAECs with upregulation of ABCG1. Conversely, ABCG1 downregulation by ABCG1 siRNA increased NADPH oxidase activity and Nox4 expression and abrogated the increase at Nrf2 nuclear protein levels. In addition, intracellular cholesterol load interfered with the balance between NADPH oxidase activity and HO-1 expression. It was suggested that ABCG1 attenuated oxidative stress induced by H2O2 in endothelial cells, which might be involved in the balance between decreased NADPH oxidase activity and increased Nrf2/OH-1 antioxidant defense signaling via its regulation for intracellular cholesterol accumulation.

scholarly journals Salidroside Improves Homocysteine-Induced Endothelial Dysfunction by Reducing Oxidative Stress

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Sin Bond Leung ◽  
Huina Zhang ◽  
Chi Wai Lau ◽  
Yu Huang ◽  
Zhixiu Lin
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Aortic Wall ◽  
Therapeutic Potential ◽  
Oxygen Species ◽  
Vascular Effect ◽  
Functional Studies ◽  
Increased Risk ◽  
No Bioavailability

Hyperhomocysteinemia is associated with an increased risk for cardiovascular diseases through increased oxidative stress. Salidroside is an active ingredient of the root ofRhodiola roseawith documented antioxidative, antihypoxia and neuroprotective properties. However, the vascular benefits of salidroside against endothelial dysfunction have yet to be explored. The present study, therefore, aimed to investigate the protective effect of salidroside on homocysteine-induced endothelial dysfunction. Functional studies on the rat aortas were performed to delineate the vascular effect of salidroside. DHE imaging was used to evaluate the reactive oxygen species (ROS) level in aortic wall and endothelial cells. Western blotting was performed to assess the protein expression associated with oxidative stress and nitric oxide (NO) bioavailability. Exposure to homocysteine attenuated endothelium-dependent relaxations in rat aortas while salidroside pretreatment rescued it. Salidroside inhibited homocystein-induced elevation in the NOX2 expression and ROS overproduction in both aortas and cultured endothelial cells and increased phosphorylation of eNOS which was diminished by homocysteine. The present study shows that salidroside is effective in preserving the NO bioavailability and thus protects against homocysteine-induced impairment of endothelium-dependent relaxations, largely through inhibiting the NOX2 expression and ROS production. Our results indicate a therapeutic potential of salidroside in the management of oxidative-stress-associated cardiovascular dysfunction.

Circulating endothelial microparticles in female migraineurs with aura

Cephalalgia ◽  
2014 ◽  
Vol 35 (2) ◽  
pp. 88-94 ◽  
Author(s):  
Thomas G Liman ◽  
Katrin Bachelier-Walenta ◽  
Lars Neeb ◽  
Jana Rosinski ◽  
Uwe Reuter ◽  
...  
Keyword(s):  
Heart Rate ◽  
Endothelial Cells ◽  
Cell Sorting ◽  
Stroke Risk ◽  
Augmentation Index ◽  
Endothelial Activation ◽  
Surface Markers ◽  
Endothelial Microparticles ◽  
Increased Risk ◽  
Control Study

Background and purpose Endothelial microparticles (EMPs) are vesicles that are released from activated endothelial cells and serve as a surrogate for endothelial dysfunction (ED). ED may be involved in migraine pathophysiology and contribute to the increased risk of ischemic stroke, particularly in female migraineurs with aura (MA). We sought to determine whether EMPs are elevated in women with MA. Methods In this case-control study, EMPs were detected by analysing surface markers using fluorescence-activated cell sorting (FACS). Surface markers were measured covering the main cell lines relevant in cardiovascular disease like endothelial cells, platelets, monocytes and leucocytes. Microparticles (MPs) were identified in correlation to calibration by 1 -µm calibrator beads (Beckman Coulter). Arterial stiffness was assessed using fingertip tonometry and the heart rate-adjusted augmentation index (AI). Results We included 29 patients with MA and 29 matched controls. MA patients had significantly higher EMPs (CD62E+AnnexinV+: 5142/µl vs 1535/µl; p < 0.001; CD144+AnnexinV+: 6683/µl vs 3107/µl; p < 0.001), monocytic (CD14+AnnexinV+ 6378 vs 3161; p < 0.001), and platelet MPs (CD62P+CD42b+AnnexinV+ 5450 vs 3204; p < 0.001). Activated EMPs (CD62E+AnnexinV+) correlated with heart-rate adjusted AI ( r = 0.46; p < 001). Conclusion EMP levels are significantly elevated in women with MA and correlated with increased AI. Our findings suggest that endothelial activation is present in women with MA. This might contribute to higher stroke risk in MA.

Short-Term Inhalation Exposure to Mild Steel Welding Fume had no Effect on Lung Inflammation and Injury but did Alter Defense Responses to Bacteria in Rats

2009 ◽  
Vol 21 (3) ◽  
pp. 182-192 ◽  
Author(s):  
James M. Antonini ◽  
Jenny R. Roberts ◽  
Sam Stone ◽  
Bean T. Chen ◽  
Diane Schwegler-Berry ◽  
...  
Keyword(s):  
Mild Steel ◽  
Lung Inflammation ◽  
Inhalation Exposure ◽  
Defense Responses ◽  
Welding Fume ◽  
Short Term ◽  
Mild Steel Welding

scholarly journals Subclinical Cardiovascular Risk Signs in Adults with Juvenile Idiopathic Arthritis in Sustained Remission

2020 ◽  
Author(s):  
Inmaculada Concepcion Aranda-Valera ◽  
Iván Arias de la Rosa ◽  
Rosa Roldan-Molina ◽  
Maria del Carmen Abalos-Aguilera ◽  
Carmen Torres-Granados ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Endothelial Cells ◽  
Endothelial Activation ◽  
Sustained Remission ◽  
Cvd Risk Factors ◽  
Cvd Risk ◽  
Activation Markers ◽  
Arterial Blood

Abstract Background:Juvenile Idiopathic Arthritis (JIA) is one of the most common chronic diseases of childhood that often persists into adulthood and can result in significant long-term morbidity. As a long lasting chronic inflammatory disease, concern has been raised regarding the risk of premature development of cardiovascular disease (CVD) in JIA. This study aims to determine whether adults with JIA in clinical remission and medium-long duration of the disease display subclinical signs of CVD risk. Methods: This is a cross-sectional study including 25 patients diagnosed with JIA according to the International League of Associations for Rheumatology criteria (ILAR 2001) and 25 age- and sex-matched controls. Remission was determined by JADAS10<1 and according to Wallace criteria. The presence of traditional CVD risk factors was analyzed. An extensive clinical analysis including body mass index (BMI), lipid profile, homeostatic model assessment – insulin resistance (HOMA-IR) and arterial blood pressure was performed. Intima media thickness of the common carotid artery (cIMT) was measured as a marker of subclinical atherosclerosis. Several proinflammatory cytokines, molecules involved in the endothelial dysfunction and adipokines were quantified on serum by ELISA. In vitro studies were carried out in healthy peripheral mononuclear cells (PBMCs), adipocytes and endothelial cells which were treated with serum from JIA patients under sustained remission. The expression of inflammatory molecules, oxidative stress and endothelial activation markers and adipokines was analyzed. Results : Mean duration of the disease was 13.47 ± 5.47 years. Mean age was 25.11 ± 7.21. Time in remission was 3.52 ± 3.33 years. CVD risk factors were similar in JIA patients and controls. However, cholesterol levels were significantly elevated in JIA patients. Serum levels of adipocytokines, oxidative stress and endothelial activation markers were elevated in serum and PBMCs from JIA patients. Serum of those JIA patients induced the activation of adipocytes, endothelial cells and healthy PBMCs. Conclusions: Long-term JIA adult patients in remission might have subclinical signs of inflammation and CVD risk, showed by an increase in the levels of inflammatory cytokines, endothelial activation and oxidative stress markers and adipokines, molecules closely involved in the alteration of the vascular system. Thus, CVD risk assessment might be considered as part of routine clinical care in those patients.

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