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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Author(s):
Girao-Silva, T. [1] ; Fonseca-Alaniz, M. H. [1] ; Ribeiro-Silva, J. C. [1] ; Lee, J. [2] ; Patil, N. P. [2] ; Dallan, L. A. [1] ; Baker, A. B. [2] ; Harmsen, M. C. [3] ; Krieger, J. E. [1] ; Miyakawa, A. A. [1]
Total Authors: 10
Affiliation:
[1] Univ Sao Paulo, Lab Genet & Mol Cardiol, Heart Inst InCor, Med Sch, Av Dr Eneas de Carvalho Aguiar, 44 Bloco 2, BR-05403000 Sao Paulo, SP - Brazil
[2] Univ Texas Austin, Dept Biomed Engn, Inst Cellular & Mol Biol, Inst Biomat Drug Delivery & Regenerat Med, Inst Co, Austin, TX - USA
[3] Univ Groningen, Univ Med Ctr Groningen, Lab Cardiovasc Regenerat Med Res Grp CAVAREM, Dept Pathol & Med Biol, Groningen - Netherlands
Total Affiliations: 3
Document type: Journal article
Source: SCIENTIFIC REPORTS; v. 11, n. 1 JUN 29 2021.
Web of Science Citations: 0
Abstract

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. (AU)

FAPESP's process: 13/17368-0 - Cardiovascular genomics: mechanisms & novel therapeutics - CVGen mech2ther
Grantee:José Eduardo Krieger
Support Opportunities: Research Projects - Thematic Grants