Role of tensile stress and strain in the induction of cell death in experimental vein grafts

M. M. Moore, J. Goldman, A. R. Patel, S. Chien, S. Q. Liu*

*Corresponding author for this work

Research output: Contribution to journalArticle

33 Scopus citations

Abstract

Tensile stress and strain are known to induce vascular cell proliferation, a process that is physiologically counterbalanced by cell death. Here we investigate whether tensile stress and strain regulate vascular-cell death by using an end-to-end anastomosed rat vein graft model. In such a model, the circumferential tensile stress in the graft wall was increased by ∼140 times immediately after surgery compared with that in the venous wall. This change was associated with an increase in the percentage of TUNEL-positive cells at 1, 6, 24, 120, 240, and 720h with two distinct peaks at 1 and 24h (10.1±3.5 and 14.4±3.2%, respectively) compared with that in control jugular veins (0.4±0.5 and 0.5±0.5% at 1 and 24h, respectively). When tensile stress and strain in the vein graft wall were reduced by using a biomechanical engineering approach, the rate of cell death was reduced significantly (3.6±1.1 and 1.6±0.5% at 1 and 24h, respectively). Furthermore, DEVD-CHO, a tetrapeptide aldehyde that inhibits the activity of caspase 3, significantly suppressed this event. These results suggest that a step increase in tensile stress and strain in experimental vein grafts induces rapid cell death, which is possibly mediated by cell death signaling mechanisms.

Original languageEnglish (US)
Pages (from-to)289-297
Number of pages9
JournalJournal of Biomechanics
Volume34
Issue number3
DOIs
StatePublished - 2001

Keywords

  • Apoptosis
  • SMC proliferation
  • Tissue engineering

ASJC Scopus subject areas

  • Biophysics
  • Orthopedics and Sports Medicine
  • Biomedical Engineering
  • Rehabilitation

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