The anti-coagulants ASIS or APC do not protect against renal ischemia/ reperfusion injury

Renal ischemia/reperfusion (I/R) injury is the main cause of acute renal failure. The severity of injury is determined by endothelial damage as well as inflammatory and apoptotic processes. The anti-coagulants active site inhibited factor VIIa (ASIS) and activated protein C (APC) are besides their a...

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Main Authors: Sarah Loubele, Arnold Spek, Peter Leenders, R A Matthijsen, Wim Buurman, carine peutz-kootstra, Hugo ten Cate, Henri Spronk
Format: Article
Language:English
Published: ScienceOpen 2014-05-01
Series:ScienceOpen Research
Online Access:https://www.scienceopen.com/document?vid=34421699-3b09-497d-bf20-61b35dfb919f
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spelling doaj-65a598f682fb4ec685583e0e3d115db02020-12-15T17:21:29ZengScienceOpenScienceOpen Research2199-10062014-05-0110.14293/S2199-1006.1.SOR-MED.AYXBIK.v1The anti-coagulants ASIS or APC do not protect against renal ischemia/ reperfusion injurySarah LoubeleArnold SpekPeter LeendersR A MatthijsenWim Buurmancarine peutz-kootstraHugo ten CateHenri SpronkRenal ischemia/reperfusion (I/R) injury is the main cause of acute renal failure. The severity of injury is determined by endothelial damage as well as inflammatory and apoptotic processes. The anti-coagulants active site inhibited factor VIIa (ASIS) and activated protein C (APC) are besides their anti-coagulant function also known for their cytoprotective properties. In this study the effect of ASIS and APC was assessed on renal I/R injury and this in relation to inflammation and apoptosis. Our results showed no effect of ASIS or APC on renal injury as determined by histopathological scoring as well as by BUN and creatinin levels. Furthermore, no effect on fibrin staining was detected but ASIS did reduce TF activity levels after a 2 hrs reperfusion period. Neither ASIS nor APC administration influenced overall inflammation markers, although some inflammatory effects of ASIS on interleukin (IL)-1β and tumor necrosis factor (TNF)-α were detectable after 2 hrs of reperfusion. Finally, neither APC nor ASIS had an influence on cell signaling pathways or on the number of apoptotic cells within the kidneys. From this study we can conclude that the anti-coagulants ASIS and APC do not have protective effects in renal I/R injury in the experimental setup as used in this study which is in contrast to the protective effects of these anti-coagulants in other models of I/R.https://www.scienceopen.com/document?vid=34421699-3b09-497d-bf20-61b35dfb919f
collection DOAJ
language English
format Article
sources DOAJ
author Sarah Loubele
Arnold Spek
Peter Leenders
R A Matthijsen
Wim Buurman
carine peutz-kootstra
Hugo ten Cate
Henri Spronk
spellingShingle Sarah Loubele
Arnold Spek
Peter Leenders
R A Matthijsen
Wim Buurman
carine peutz-kootstra
Hugo ten Cate
Henri Spronk
The anti-coagulants ASIS or APC do not protect against renal ischemia/ reperfusion injury
ScienceOpen Research
author_facet Sarah Loubele
Arnold Spek
Peter Leenders
R A Matthijsen
Wim Buurman
carine peutz-kootstra
Hugo ten Cate
Henri Spronk
author_sort Sarah Loubele
title The anti-coagulants ASIS or APC do not protect against renal ischemia/ reperfusion injury
title_short The anti-coagulants ASIS or APC do not protect against renal ischemia/ reperfusion injury
title_full The anti-coagulants ASIS or APC do not protect against renal ischemia/ reperfusion injury
title_fullStr The anti-coagulants ASIS or APC do not protect against renal ischemia/ reperfusion injury
title_full_unstemmed The anti-coagulants ASIS or APC do not protect against renal ischemia/ reperfusion injury
title_sort anti-coagulants asis or apc do not protect against renal ischemia/ reperfusion injury
publisher ScienceOpen
series ScienceOpen Research
issn 2199-1006
publishDate 2014-05-01
description Renal ischemia/reperfusion (I/R) injury is the main cause of acute renal failure. The severity of injury is determined by endothelial damage as well as inflammatory and apoptotic processes. The anti-coagulants active site inhibited factor VIIa (ASIS) and activated protein C (APC) are besides their anti-coagulant function also known for their cytoprotective properties. In this study the effect of ASIS and APC was assessed on renal I/R injury and this in relation to inflammation and apoptosis. Our results showed no effect of ASIS or APC on renal injury as determined by histopathological scoring as well as by BUN and creatinin levels. Furthermore, no effect on fibrin staining was detected but ASIS did reduce TF activity levels after a 2 hrs reperfusion period. Neither ASIS nor APC administration influenced overall inflammation markers, although some inflammatory effects of ASIS on interleukin (IL)-1β and tumor necrosis factor (TNF)-α were detectable after 2 hrs of reperfusion. Finally, neither APC nor ASIS had an influence on cell signaling pathways or on the number of apoptotic cells within the kidneys. From this study we can conclude that the anti-coagulants ASIS and APC do not have protective effects in renal I/R injury in the experimental setup as used in this study which is in contrast to the protective effects of these anti-coagulants in other models of I/R.
url https://www.scienceopen.com/document?vid=34421699-3b09-497d-bf20-61b35dfb919f
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