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Arterial Blood Pressure Induces Transient C4b-Binding Protein in Human Saphenous Vein Grafts

Kupreishvili, Koba; Meischl, Christof; Vonk, Alexander B. A.; Stooker, Wim; Eijsman, Leon; Blom, Anna M. LU ; Quax, Paul H A; van Hinsbergh, Victor W M; Niessen, Hans W M and Krijnen, Paul A. J. (2017) In Annals of Vascular Surgery 41. p.259-264
Abstract

Background: Complement is an important mediator in arterial blood pressure-induced vein graft failure. Previously, we noted activation of cell protective mechanisms in human saphenous veins too. Here we have analyzed whether C4b-binding protein (C4bp), an endogenous complement inhibitor, is present in the vein wall. Methods: Human saphenous vein segments obtained from patients undergoing coronary artery bypass grafting (n = 55) were perfused in vitro at arterial blood pressure with either autologous blood for 1, 2, 4, or 6 hr or with autologous blood supplemented with reactive oxygen species scavenger N-acetylcysteine. The segments were subsequently analyzed quantitatively for presence of C4bp and complement activation product C3d using... (More)

Background: Complement is an important mediator in arterial blood pressure-induced vein graft failure. Previously, we noted activation of cell protective mechanisms in human saphenous veins too. Here we have analyzed whether C4b-binding protein (C4bp), an endogenous complement inhibitor, is present in the vein wall. Methods: Human saphenous vein segments obtained from patients undergoing coronary artery bypass grafting (n = 55) were perfused in vitro at arterial blood pressure with either autologous blood for 1, 2, 4, or 6 hr or with autologous blood supplemented with reactive oxygen species scavenger N-acetylcysteine. The segments were subsequently analyzed quantitatively for presence of C4bp and complement activation product C3d using immunohistochemistry. Results: Perfusion induced deposition of C3d and C4bp within the media of the vessel wall, which increased reproducibly and significantly over a period of 4 hr up to 3.8% for C3d and 81% for C4bp of the total vessel area. Remarkably after 6 hr of perfusion, the C3d-positive area decreased significantly to 1.3% and the C4bp-positive area to 19% of the total area of the vein. The areas positive for both C4bp and C3d were increased in the presence of N-acetylcysteine. Conclusions: Exposure to arterial blood pressure leads to a transient presence of C4bp in the vein wall. This may be part of a cell-protective mechanism to counteract arterial blood pressure-induced cellular stress and inflammation in grafted veins.

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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Annals of Vascular Surgery
volume
41
pages
259 - 264
publisher
Springer
external identifiers
  • scopus:85013042085
  • wos:000402642100046
ISSN
0890-5096
DOI
10.1016/j.avsg.2016.10.033
language
English
LU publication?
yes
id
6cea802e-cf81-425b-9d54-fdf1351caea5
date added to LUP
2017-03-03 13:13:05
date last changed
2018-01-07 11:54:00
@article{6cea802e-cf81-425b-9d54-fdf1351caea5,
  abstract     = {<p>Background: Complement is an important mediator in arterial blood pressure-induced vein graft failure. Previously, we noted activation of cell protective mechanisms in human saphenous veins too. Here we have analyzed whether C4b-binding protein (C4bp), an endogenous complement inhibitor, is present in the vein wall. Methods: Human saphenous vein segments obtained from patients undergoing coronary artery bypass grafting (n = 55) were perfused in vitro at arterial blood pressure with either autologous blood for 1, 2, 4, or 6 hr or with autologous blood supplemented with reactive oxygen species scavenger N-acetylcysteine. The segments were subsequently analyzed quantitatively for presence of C4bp and complement activation product C3d using immunohistochemistry. Results: Perfusion induced deposition of C3d and C4bp within the media of the vessel wall, which increased reproducibly and significantly over a period of 4 hr up to 3.8% for C3d and 81% for C4bp of the total vessel area. Remarkably after 6 hr of perfusion, the C3d-positive area decreased significantly to 1.3% and the C4bp-positive area to 19% of the total area of the vein. The areas positive for both C4bp and C3d were increased in the presence of N-acetylcysteine. Conclusions: Exposure to arterial blood pressure leads to a transient presence of C4bp in the vein wall. This may be part of a cell-protective mechanism to counteract arterial blood pressure-induced cellular stress and inflammation in grafted veins.</p>},
  author       = {Kupreishvili, Koba and Meischl, Christof and Vonk, Alexander B. A. and Stooker, Wim and Eijsman, Leon and Blom, Anna M. and Quax, Paul H A and van Hinsbergh, Victor W M and Niessen, Hans W M and Krijnen, Paul A. J.},
  issn         = {0890-5096},
  language     = {eng},
  pages        = {259--264},
  publisher    = {Springer},
  series       = {Annals of Vascular Surgery},
  title        = {Arterial Blood Pressure Induces Transient C4b-Binding Protein in Human Saphenous Vein Grafts},
  url          = {http://dx.doi.org/10.1016/j.avsg.2016.10.033},
  volume       = {41},
  year         = {2017},
}