Subarachnoid Hemorrhage Increases Level of Heme Oxygenase-1 and Biliverdin Reductase in the Choroid Plexus

Subarachnoid hemorrhage is a specific, life-threatening form of hemorrhagic stroke linked to high morbidity and mortality. It has been found that the choroid plexus of the brain ventricles forming the blood-cerebrospinal fluid barrier plays an important role in subarachnoid hemorrhage pathophysiolog...

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Main Authors: Peter Solár, Václav Brázda, Shahaf Levin, Alemeh Zamani, Radim Jančálek, Petr Dubový, Marek Joukal
Format: Article
Language:English
Published: Frontiers Media S.A. 2020-11-01
Series:Frontiers in Cellular Neuroscience
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fncel.2020.593305/full
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author Peter Solár
Peter Solár
Peter Solár
Václav Brázda
Václav Brázda
Shahaf Levin
Alemeh Zamani
Radim Jančálek
Radim Jančálek
Petr Dubový
Marek Joukal
author_facet Peter Solár
Peter Solár
Peter Solár
Václav Brázda
Václav Brázda
Shahaf Levin
Alemeh Zamani
Radim Jančálek
Radim Jančálek
Petr Dubový
Marek Joukal
author_sort Peter Solár
collection DOAJ
description Subarachnoid hemorrhage is a specific, life-threatening form of hemorrhagic stroke linked to high morbidity and mortality. It has been found that the choroid plexus of the brain ventricles forming the blood-cerebrospinal fluid barrier plays an important role in subarachnoid hemorrhage pathophysiology. Heme oxygenase-1 and biliverdin reductase are two of the key enzymes of the hemoglobin degradation cascade. Therefore, the aim of present study was to investigate changes in protein levels of heme oxygenase-1 and biliverdin reductase in the rat choroid plexus after experimental subarachnoid hemorrhage induced by injection of non-heparinized autologous blood to the cisterna magna. Artificial cerebrospinal fluid of the same volume as autologous blood was injected to mimic increased intracranial pressure in control rats. Immunohistochemical and Western blot analyses were used to monitor changes in the of heme oxygenase-1 and biliverdin reductase levels in the rat choroid plexus after induction of subarachnoid hemorrhage or artificial cerebrospinal fluid application for 1, 3, and 7 days. We found increased levels of heme oxygenase-1 and biliverdin reductase protein in the choroid plexus over the entire period following subarachnoid hemorrhage induction. The level of heme oxygenase-1 was the highest early (1 and 3 days) after subarachnoid hemorrhage indicating its importance in hemoglobin degradation. Increased levels of heme oxygenase-1 were also observed in the choroid plexus epithelial cells at all time points after application of artificial cerebrospinal fluid. Biliverdin reductase protein was detected mainly in the choroid plexus epithelial cells, with levels gradually increasing during subarachnoid hemorrhage. Our results suggest that heme oxygenase-1 and biliverdin reductase are involved not only in hemoglobin degradation but probably also in protecting choroid plexus epithelial cells and the blood-cerebrospinal fluid barrier from the negative effects of subarachnoid hemorrhage.
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spelling doaj.art-09c1922dce144879800fd97c9f79acaa2022-12-21T22:08:44ZengFrontiers Media S.A.Frontiers in Cellular Neuroscience1662-51022020-11-011410.3389/fncel.2020.593305593305Subarachnoid Hemorrhage Increases Level of Heme Oxygenase-1 and Biliverdin Reductase in the Choroid PlexusPeter Solár0Peter Solár1Peter Solár2Václav Brázda3Václav Brázda4Shahaf Levin5Alemeh Zamani6Radim Jančálek7Radim Jančálek8Petr Dubový9Marek Joukal10Department of Anatomy, Faculty of Medicine, Cellular and Molecular Neurobiology Research Group, Masaryk University, Brno, CzechiaDepartment of Neurosurgery – St. Anne’s University Hospital Brno, Faculty of Medicine, Masaryk University, Brno, CzechiaDepartment of Neurosurgery, St. Anne’s University Hospital Brno, Brno, CzechiaDepartment of Anatomy, Faculty of Medicine, Cellular and Molecular Neurobiology Research Group, Masaryk University, Brno, CzechiaInstitute of Biophysics of the Czech Academy of Sciences, Brno, CzechiaDepartment of Anatomy, Faculty of Medicine, Cellular and Molecular Neurobiology Research Group, Masaryk University, Brno, CzechiaDepartment of Anatomy, Faculty of Medicine, Cellular and Molecular Neurobiology Research Group, Masaryk University, Brno, CzechiaDepartment of Neurosurgery – St. Anne’s University Hospital Brno, Faculty of Medicine, Masaryk University, Brno, CzechiaDepartment of Neurosurgery, St. Anne’s University Hospital Brno, Brno, CzechiaDepartment of Anatomy, Faculty of Medicine, Cellular and Molecular Neurobiology Research Group, Masaryk University, Brno, CzechiaDepartment of Anatomy, Faculty of Medicine, Cellular and Molecular Neurobiology Research Group, Masaryk University, Brno, CzechiaSubarachnoid hemorrhage is a specific, life-threatening form of hemorrhagic stroke linked to high morbidity and mortality. It has been found that the choroid plexus of the brain ventricles forming the blood-cerebrospinal fluid barrier plays an important role in subarachnoid hemorrhage pathophysiology. Heme oxygenase-1 and biliverdin reductase are two of the key enzymes of the hemoglobin degradation cascade. Therefore, the aim of present study was to investigate changes in protein levels of heme oxygenase-1 and biliverdin reductase in the rat choroid plexus after experimental subarachnoid hemorrhage induced by injection of non-heparinized autologous blood to the cisterna magna. Artificial cerebrospinal fluid of the same volume as autologous blood was injected to mimic increased intracranial pressure in control rats. Immunohistochemical and Western blot analyses were used to monitor changes in the of heme oxygenase-1 and biliverdin reductase levels in the rat choroid plexus after induction of subarachnoid hemorrhage or artificial cerebrospinal fluid application for 1, 3, and 7 days. We found increased levels of heme oxygenase-1 and biliverdin reductase protein in the choroid plexus over the entire period following subarachnoid hemorrhage induction. The level of heme oxygenase-1 was the highest early (1 and 3 days) after subarachnoid hemorrhage indicating its importance in hemoglobin degradation. Increased levels of heme oxygenase-1 were also observed in the choroid plexus epithelial cells at all time points after application of artificial cerebrospinal fluid. Biliverdin reductase protein was detected mainly in the choroid plexus epithelial cells, with levels gradually increasing during subarachnoid hemorrhage. Our results suggest that heme oxygenase-1 and biliverdin reductase are involved not only in hemoglobin degradation but probably also in protecting choroid plexus epithelial cells and the blood-cerebrospinal fluid barrier from the negative effects of subarachnoid hemorrhage.https://www.frontiersin.org/articles/10.3389/fncel.2020.593305/fullsubarachnoid hemorrhagechoroid plexusheme oxygenase-1biliverdin reductasemacrophages
spellingShingle Peter Solár
Peter Solár
Peter Solár
Václav Brázda
Václav Brázda
Shahaf Levin
Alemeh Zamani
Radim Jančálek
Radim Jančálek
Petr Dubový
Marek Joukal
Subarachnoid Hemorrhage Increases Level of Heme Oxygenase-1 and Biliverdin Reductase in the Choroid Plexus
Frontiers in Cellular Neuroscience
subarachnoid hemorrhage
choroid plexus
heme oxygenase-1
biliverdin reductase
macrophages
title Subarachnoid Hemorrhage Increases Level of Heme Oxygenase-1 and Biliverdin Reductase in the Choroid Plexus
title_full Subarachnoid Hemorrhage Increases Level of Heme Oxygenase-1 and Biliverdin Reductase in the Choroid Plexus
title_fullStr Subarachnoid Hemorrhage Increases Level of Heme Oxygenase-1 and Biliverdin Reductase in the Choroid Plexus
title_full_unstemmed Subarachnoid Hemorrhage Increases Level of Heme Oxygenase-1 and Biliverdin Reductase in the Choroid Plexus
title_short Subarachnoid Hemorrhage Increases Level of Heme Oxygenase-1 and Biliverdin Reductase in the Choroid Plexus
title_sort subarachnoid hemorrhage increases level of heme oxygenase 1 and biliverdin reductase in the choroid plexus
topic subarachnoid hemorrhage
choroid plexus
heme oxygenase-1
biliverdin reductase
macrophages
url https://www.frontiersin.org/articles/10.3389/fncel.2020.593305/full
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