scholarly journals A Water-Soluble Fullerene Vesicle Alleviates Angiotensin II-Induced Oxidative Stress in Human Umbilical Venous Endothelial Cells

2008 ◽  
Vol 31 (1) ◽  
pp. 141-151 ◽  
Author(s):  
Rui MAEDA ◽  
Eisei NOIRI ◽  
Hiroyuki ISOBE ◽  
Tatsuya HOMMA ◽  
Tamami TANAKA ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Angiotensin Ii ◽  
Water Soluble

Oxidative stress induced by urban fine particles in cultured EA.hy926 cells

2010 ◽  
Vol 30 (7) ◽  
pp. 579-590 ◽  
Author(s):  
Han Wei ◽  
Dan Wei ◽  
Shuo Yi ◽  
Fang Zhang ◽  
Wenjun Ding
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Fine Particles ◽  
Cell Damage ◽  
Umbilical Vein ◽  
Direct Interaction ◽  
Water Soluble ◽  
Apoptotic Pathway ◽  
Metal Elements ◽  
Ea.Hy926 Cells

It has been reported that vascular endothelia cell damage is an important precursor to the morbidity and mortality associated with cardiovascular disease exposed to airborne particulate matter (PM). The present study investigated the hypothesis that urban fine (PM2.5) particles could cause cytotoxicity via oxidative stress in human umbilical vein endothelial cells, EA.hy926. The concentrations of metal elements (Cr, Fe, Ni, Cu, Zn, Mo, Cd and Pb) in PM2.5 suspension, water-soluble and water-insoluble fractions of PM2.5 were determined by inductively coupled plasma - mass spectrometry (ICP-MS). Iron (Fe), Zn and Pb were highly enriched in all the samples. Exposure of the cultured EA.hy926 cells to PM2.5 suspension, water-soluble and water-insoluble fractions of PM2.5 led to cell death, reactive oxygen species (ROS) increase, mitochondrial transmembrane potential (ΔΨm) disruption and NF-κB activation, respectively. The ROS increase by exposure to PM 2.5 suspension, water-soluble and water-insoluble fractions of PM 2.5 triggered the activation of nuclear factor (NF)-κB, which means that PM2.5 particles exert cytotoxicity by an apopotic process. However, the induction of cytotoxicity by PM2.5 suspension, water-soluble and water-insoluble fractions of PM2.5 was reversed by pretreatment with superoxide dismutase (SOD). These results suggest that each fraction of PM2.5 has a potency to cause oxidative stress in endothelial cells. ROS was generated through PM2.5-mediated mitochondrial apoptotic pathway, which may induce direct interaction between metal elements and endothelia cells.

P6266Circulating microparticules of patients with coronary artery disease up-regulate the expression of sodium-glucose cotransporters 1 and 2 in coronary artery endothelial cells: role of angiotensin II

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Park ◽  
E Belcastro ◽  
H Hasan ◽  
C Bruckert ◽  
B Marchandot ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Endothelial Cells ◽  
Coronary Artery ◽  
Angiotensin Ii ◽  
Endothelial Dysfunction ◽  
Protein Level ◽  
Immunocytochemical Staining ◽  
Ang Ii ◽  
Angiotensin System

Abstract Introduction Circulating microparticles (MPs) from patients with coronary artery diseases (CAD) have been shown to promote endothelial senescence and dysfunction involving the pro-oxidant local angiotensin system. Sodium-glucose cotransporters (SGLTs)2 inhibitors decreased the risk of cardiovascular disease in patients with type 2 diabetes and this effect appears to be independent of glycemic control. Moreover, high glucose and H2O2 have been shown to cause a redox-sensitive upregulation of SGLT1 and 2 in coronary artery endothelial cells (ECs). Aim Therefore, this study examined whether angiotensin II (Ang II, a potent NADPH oxidase-dependent inducer of oxidative stress) and CAD MPs stimulate SGLT1 and 2 expression in ECs, and assessed their role in the induction of endothelial dysfunction. Methods ECs were isolated from porcine coronary arteries. The protein expression level was assessed by Western blot analysis and immunocytochemical staining, oxidative stress using dihydroethidium staining, and senescence by senescence-associated beta-galactosidase activity (SA-beta-gal activity). Circulating CAD MPs were collected from blood samples of patients (61–79 year) with established cardiovascular disease. Results Control ECs expressed low levels of SGLT1 and SGLT2 proteins. Exposure of ECs to Ang II caused a time- and concentration-dependent increase in the protein level of SGLT1 and SGLT2 with a significant increase observed at concentrations as low as 10 nM. Exposure of ECs to CAD MPs (10 nM PhtdSer eq) from 3/5 patients increased the SGLT1 and SGLT2 protein level. An increased SGLT1 and SGLT2 immunofluorescence signal was also observed in response to Ang II and H2O2. Ang II increased the level of oxidative stress, SA-beta-gal activity, senescence markers (p53, p21 and p16), VCAM-1, MCP-1, tissue factor (TF) and the local angiotensin system (ACE, AT1R), and down-regulated that of eNOS. CAD MPs from 4/5 patients decreased eNOS level and from 5/5 patients increased VCAM-1 level. All the Ang II-induced effects were prevented by the dual SGLT1/2 inhibitor LX-4211 and the selective SGLT2 inhibitor, empagliflozin. Conclusions The present findings indicate that CAD MPs and Ang II upregulate the expression of SGLT1 and SGLT2 protein levels in ECs, and that they promote endothelial dysfunction. They further suggest that inhibition of SGLT1 and/or SGLT2 might be an attractive strategy to protect the arterial wall and, hence, the development of cardiovascular diseases. Acknowledgement/Funding Unrestricted research grant from Boehringer Ingelheim Pharma GmbH & Co. KG

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