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

• DOI: 10.1038/s41598-021-93081-3
• Publication Date: 2021-06-29T10:07:24Z
• Authors: T. Girão-Silva; M. H. Fonseca-Alaniz; J. C. Ribeiro-Silva; J. Lee; N. P. Patil; L. A. Dallan; A. B. Baker; M. C. Harmsen; J. E. Krieger; A. A. Miyakawa
• Keywords: Endothelial Dysfunction; Stress fiber

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