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.
(Less)
- author
- 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.
- organization
- publishing date
- 2017
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Annals of Vascular Surgery
- volume
- 41
- pages
- 259 - 264
- publisher
- Springer
- external identifiers
-
- pmid:28163174
- wos:000402642100046
- scopus:85013042085
- 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
- 2025-01-07 09:03:32
@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}},
doi = {{10.1016/j.avsg.2016.10.033}},
volume = {{41}},
year = {{2017}},
}