High stretch induces endothelial dysfunction accompanied by oxidative stress and actin remodeling in human saphenous vein endothelial cells

The 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) dysfunct...

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Published inScientific reports Vol. 11; no. 1; p. 13493
Main Authors Girão-Silva, T., Fonseca-Alaniz, M. H., Ribeiro-Silva, J. C., Lee, J., Patil, N. P., Dallan, L. A., Baker, A. B., Harmsen, M. C., Krieger, J. E., Miyakawa, A. A.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 29.06.2021
Nature Publishing Group
Nature Portfolio
Subjects
631/80
631/80/86
692/4019
692/4019/592
Acetylcysteine
Actin
Adhesion
Antioxidants
Bioavailability
Cell adhesion
Cofilin
Coronary artery
Cytoskeleton
E-selectin
Endothelial cells
Heart surgery
Humanities and Social Sciences
Inflammation
multidisciplinary
Oxidative stress
Science
Science (multidisciplinary)
Veins & arteries
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Summary:The 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.
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ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-021-93081-3