scholarly journals The Effects of Pitavastatin on Nuclear Factor-Kappa B and ICAM-1 in Human Saphenous Vein Graft Endothelial Culture

2019 ◽  
Vol 2019 ◽  
pp. 1-12
Author(s):  
Bulent Demir ◽  
Burak Onal ◽  
Sibel Ozyazgan ◽  
Esra Demir ◽  
Vedat Bakuy ◽  
...  

Objective. To study pitavastatin’s effects on nuclear factor-kappa B (NF-κB ) and adhesion molecules in human saphenous vein graft endothelial culture indicating its pleotropic properties. Materials and Method. Low-dose (0.1 μM/L) and high-dose (1μM/L) pitavastatin calcium were administered as a frontline therapy in human saphenous endothelial cell culture, followed by induction of inflammation by TNF-α and determination of mRNA level alterations of ICAM-1 and NF-κB genes of endothelial cells using the qRT-PCR method. Additionally, immunofluorescence method was used to show the expression of NF-κB and ICAM-1. Finally, LDH levels were determined by the ELISA method to quantify cytotoxicity. Results. ICAM-1 mRNA expression in the low-dose pitavastatin+TNF-α group was significantly higher than that in the TNF-α group and significantly lower than that in the high-dose pitavastatin+TNF-α group (for all comparisons, P = 0.001). The low-dose pitavastatin+TNF-α group had a similar NF-κB mRNA expression with TNF-α and high-dose pitavastatin+TNF-α groups. Conclusion. Pitavastatin increases ICAM-1 mRNA expression in saphenous vein endothelial cells. Furthermore, the effect of pitavastatin on adhesion molecules appears independent of NF-κB. Novel studies are needed in this field.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
T. Girão-Silva ◽  
M. H. Fonseca-Alaniz ◽  
J. C. Ribeiro-Silva ◽  
J. Lee ◽  
N. P. Patil ◽  
...  

AbstractThe rate of the remodeling of the arterialized saphenous vein conduit limits the outcomes of coronary artery bypass graft surgery (CABG), which may be influenced by endothelial dysfunction. We tested the hypothesis that high stretch (HS) induces human saphenous vein endothelial cell (hSVEC) dysfunction and examined candidate underlying mechanisms. Our results showed that in vitro HS reduces NO bioavailability, increases inflammatory adhesion molecule expression (E-selectin and VCAM1) and THP-1 cell adhesion. HS decreases F-actin in hSVECs, but not in human arterial endothelial cells, and is accompanied by G-actin and cofilin’s nuclear shuttling and increased reactive oxidative species (ROS). Pre-treatment with the broad-acting antioxidant N-acetylcysteine (NAC) supported this observation and diminished stretch-induced actin remodeling and inflammatory adhesive molecule expression. Altogether, we provide evidence that increased oxidative stress and actin cytoskeleton remodeling play a role in HS-induced saphenous vein endothelial cell dysfunction, which may contribute to predisposing saphenous vein graft to failure.


2018 ◽  
Vol 39 (suppl_1) ◽  
Author(s):  
M S Ruiter ◽  
G Garoffolo ◽  
M Piola ◽  
M Agrifoglio ◽  
M Zanobini ◽  
...  

1999 ◽  
Vol 83 (12) ◽  
pp. 1623-1628 ◽  
Author(s):  
Paul S Teirstein ◽  
J.Tift Mann ◽  
Paul E Cundey ◽  
Eliot Schechter ◽  
W.Carlisle Jacobs ◽  
...  

2011 ◽  
Vol 666 (1-3) ◽  
pp. 150-157 ◽  
Author(s):  
Naciye Yaktubay Döndaş ◽  
Nehir Sucu ◽  
Banu Coşkun Yilmaz ◽  
Halil Mahir Kaplan ◽  
Murat Özeren ◽  
...  

2002 ◽  
Vol 21 (2) ◽  
pp. 212-217 ◽  
Author(s):  
W. Stooker ◽  
H.W.M. Niessen ◽  
W.R. Wildevuur ◽  
V.W.M. van Hinsbergh ◽  
J. Fritz ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Anna C. Roberts ◽  
Jai Gohil ◽  
Laura Hudson ◽  
Kyle Connolly ◽  
Philip Warburton ◽  
...  

Type 2 diabetes (T2DM) confers increased risk of endothelial dysfunction, coronary heart disease, and vulnerability to vein graft failure after bypass grafting, despite glycaemic control. This study explored the concept that endothelial cells (EC) cultured from T2DM and nondiabetic (ND) patients are phenotypically and functionally distinct. Cultured human saphenous vein- (SV-) EC were compared between T2DM and ND patients in parallel. Proliferation, migration, andin vitroangiogenesis assays were performed; western blotting was used to quantify phosphorylation of Akt, ERK, and eNOS. The ability of diabetic stimuli (hyperglycaemia, TNF-α, and palmitate) to modulate angiogenic potential of ND-EC was also explored. T2DM-EC displayed reduced migration (~30%) and angiogenesis (~40%) compared with ND-EC and a modest, nonsignificant trend to reduced proliferation. Significant inhibition of Akt and eNOS, but not ERK phosphorylation, was observed in T2DM cells. Hyperglycaemia did not modify ND-EC function, but TNF-αand palmitate significantly reduced angiogenic capacity (by 27% and 43%, resp.), effects mimicked by Akt inhibition. Aberrancies of EC function may help to explain the increased risk of SV graft failure in T2DM patients. This study highlights the importance of other potentially contributing factors in addition to hyperglycaemia that may inflict injury and long-term dysfunction to the homeostatic capacity of the endothelium.


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