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

Koba Kupreishvili, Christof Meischl, Alexander B A Vonk, Wim Stooker, Leon Eijsman, Anna M Blom, Paul H A Quax, Victor W M van Hinsbergh, Hans W M Niessen, Paul A J Krijnen

Research output: Contribution to journalArticleAcademicpeer-review

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 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.

Original languageEnglish
Pages (from-to)259-264
Number of pages6
JournalAnnals of Vascular Surgery
Volume41
DOIs
Publication statusPublished - May 2017

Cite this

Kupreishvili, Koba ; Meischl, Christof ; Vonk, Alexander B A ; Stooker, Wim ; Eijsman, Leon ; Blom, Anna M ; Quax, Paul H A ; van Hinsbergh, Victor W M ; Niessen, Hans W M ; Krijnen, Paul A J. / Arterial Blood Pressure Induces Transient C4b-Binding Protein in Human Saphenous Vein Grafts. In: Annals of Vascular Surgery. 2017 ; Vol. 41. pp. 259-264.
@article{7fa6a557589f43a5a503330b1c4b4733,
title = "Arterial Blood Pressure Induces Transient C4b-Binding Protein in Human Saphenous Vein Grafts",
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 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.",
keywords = "Journal Article",
author = "Koba Kupreishvili and Christof Meischl and Vonk, {Alexander B A} and Wim Stooker and Leon Eijsman 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}",
note = "Copyright {\circledC} 2017 Elsevier Inc. All rights reserved.",
year = "2017",
month = "5",
doi = "10.1016/j.avsg.2016.10.033",
language = "English",
volume = "41",
pages = "259--264",
journal = "Annals of Vascular Surgery",
issn = "0890-5096",
publisher = "Elsevier Inc.",

}

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; Quax, Paul H A; van Hinsbergh, Victor W M; Niessen, Hans W M; Krijnen, Paul A J.

In: Annals of Vascular Surgery, Vol. 41, 05.2017, p. 259-264.

Research output: Contribution to journalArticleAcademicpeer-review

TY - JOUR

T1 - Arterial Blood Pressure Induces Transient C4b-Binding Protein in Human Saphenous Vein Grafts

AU - Kupreishvili, Koba

AU - Meischl, Christof

AU - Vonk, Alexander B A

AU - Stooker, Wim

AU - Eijsman, Leon

AU - Blom, Anna M

AU - Quax, Paul H A

AU - van Hinsbergh, Victor W M

AU - Niessen, Hans W M

AU - Krijnen, Paul A J

N1 - Copyright © 2017 Elsevier Inc. All rights reserved.

PY - 2017/5

Y1 - 2017/5

N2 - 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.

AB - 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.

KW - Journal Article

U2 - 10.1016/j.avsg.2016.10.033

DO - 10.1016/j.avsg.2016.10.033

M3 - Article

VL - 41

SP - 259

EP - 264

JO - Annals of Vascular Surgery

JF - Annals of Vascular Surgery

SN - 0890-5096

ER -