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

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Autor(es):
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]
Número total de Autores: 10
Afiliação do(s) autor(es):
[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
Número total de Afiliações: 3
Tipo de documento: Artigo Científico
Fonte: SCIENTIFIC REPORTS; v. 11, n. 1 JUN 29 2021.
Citações Web of Science: 0
Resumo

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)

Processo FAPESP: 13/17368-0 - Genômica cardiovascular: mechanismos & novas terapias - CVGen mech2ther
Beneficiário:José Eduardo Krieger
Modalidade de apoio: Auxílio à Pesquisa - Temático