Blood Progenitor Cell Mobilization Driven by TWEAK Promotes Neovascularization and Reduces Brain Damage in a Rat Model of Intracerebral Hemorrhage

Non-traumatic intracerebral hemorrhage (ICH) is one of the most devastating and disabling forms of stroke; however, there are no effective pharmacological therapies available following the insult. Angiogenesis appears as a key step to overcoming the damage and promoting functional recovery. In this...

Full description

Saved in:
Bibliographic Details
Main Authors: Daniel Romaus-Sanjurjo, Esteban López-Arias, Cristina Rodríguez, Pablo Hervella, Mariña Rodríguez-Arrizabalaga, Manuel Debasa-Mouce, Juan Manuel Pías-Peleteiro, Ramón Iglesias-Rey, Pablo Aguiar, Ángeles Almeida, José Castillo, Alberto Ouro, Tomás Sobrino
Format: Article
Language:English
Published: MDPI AG 2025-05-01
Series:Antioxidants
Subjects:
Online Access:https://www.mdpi.com/2076-3921/14/5/601
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850127456802963456
author Daniel Romaus-Sanjurjo
Esteban López-Arias
Cristina Rodríguez
Pablo Hervella
Mariña Rodríguez-Arrizabalaga
Manuel Debasa-Mouce
Juan Manuel Pías-Peleteiro
Ramón Iglesias-Rey
Pablo Aguiar
Ángeles Almeida
José Castillo
Alberto Ouro
Tomás Sobrino
author_facet Daniel Romaus-Sanjurjo
Esteban López-Arias
Cristina Rodríguez
Pablo Hervella
Mariña Rodríguez-Arrizabalaga
Manuel Debasa-Mouce
Juan Manuel Pías-Peleteiro
Ramón Iglesias-Rey
Pablo Aguiar
Ángeles Almeida
José Castillo
Alberto Ouro
Tomás Sobrino
author_sort Daniel Romaus-Sanjurjo
collection DOAJ
description Non-traumatic intracerebral hemorrhage (ICH) is one of the most devastating and disabling forms of stroke; however, there are no effective pharmacological therapies available following the insult. Angiogenesis appears as a key step to overcoming the damage and promoting functional recovery. In this context, endothelial progenitor cells (EPCs) mobilization improves oxidative stress and promotes neovascularization, which has been linked to beneficial outcomes following both ischemic and hemorrhagic stroke. The TNF-like weak inducer of apoptosis (TWEAK), binding to its receptor Fn14, has been suggested as an inducer of EPCs differentiation, viability and migration to the injury site in a model of myocardial infarction. Here, we have performed a proof-of-concept preclinical study in a rat model of ICH where we report that a 50 μg/kg dose of rat recombinant TWEAK (rTWEAK) promotes blood progenitor cells mobilization, mainly EPCs. As soon as 72 h post-injury, brain neovascularization, and, importantly, long-term hematoma reduction and improved functional recovery is reported. In contrast, a higher dose of 150 μg/kg blocked those beneficial outcomes. Therefore, a low dose of rTWEAK treatment promotes neovascularization and reduces brain damage in a rat model of ICH. Further clinical studies will be needed to demonstrate if rTWEAK could represent a new strategy to promote recovery following ICH.
format Article
id doaj-art-89875292a9914ee7bfe1d4c43059053e
institution OA Journals
issn 2076-3921
language English
publishDate 2025-05-01
publisher MDPI AG
record_format Article
series Antioxidants
spelling doaj-art-89875292a9914ee7bfe1d4c43059053e2025-08-20T02:33:39ZengMDPI AGAntioxidants2076-39212025-05-0114560110.3390/antiox14050601Blood Progenitor Cell Mobilization Driven by TWEAK Promotes Neovascularization and Reduces Brain Damage in a Rat Model of Intracerebral HemorrhageDaniel Romaus-Sanjurjo0Esteban López-Arias1Cristina Rodríguez2Pablo Hervella3Mariña Rodríguez-Arrizabalaga4Manuel Debasa-Mouce5Juan Manuel Pías-Peleteiro6Ramón Iglesias-Rey7Pablo Aguiar8Ángeles Almeida9José Castillo10Alberto Ouro11Tomás Sobrino12NeuroAging Group Laboratory (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group Laboratory (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainInstitute of Biomedical Research of Salamanca (IBSAL), University Hospital of Salamanca, CSIC, University of Salamanca, 37007 Salamanca, SpainNeuroimaging and Biotechnology Laboratory (NOBEL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group Laboratory (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group Laboratory (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group Laboratory (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroimaging and Biotechnology Laboratory (NOBEL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainCentro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Instituto de Salud Carlos III, 28029 Madrid, SpainInstitute of Biomedical Research of Salamanca (IBSAL), University Hospital of Salamanca, CSIC, University of Salamanca, 37007 Salamanca, SpainNeuroimaging and Biotechnology Laboratory (NOBEL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group Laboratory (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group Laboratory (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNon-traumatic intracerebral hemorrhage (ICH) is one of the most devastating and disabling forms of stroke; however, there are no effective pharmacological therapies available following the insult. Angiogenesis appears as a key step to overcoming the damage and promoting functional recovery. In this context, endothelial progenitor cells (EPCs) mobilization improves oxidative stress and promotes neovascularization, which has been linked to beneficial outcomes following both ischemic and hemorrhagic stroke. The TNF-like weak inducer of apoptosis (TWEAK), binding to its receptor Fn14, has been suggested as an inducer of EPCs differentiation, viability and migration to the injury site in a model of myocardial infarction. Here, we have performed a proof-of-concept preclinical study in a rat model of ICH where we report that a 50 μg/kg dose of rat recombinant TWEAK (rTWEAK) promotes blood progenitor cells mobilization, mainly EPCs. As soon as 72 h post-injury, brain neovascularization, and, importantly, long-term hematoma reduction and improved functional recovery is reported. In contrast, a higher dose of 150 μg/kg blocked those beneficial outcomes. Therefore, a low dose of rTWEAK treatment promotes neovascularization and reduces brain damage in a rat model of ICH. Further clinical studies will be needed to demonstrate if rTWEAK could represent a new strategy to promote recovery following ICH.https://www.mdpi.com/2076-3921/14/5/601endothelial progenitor cellsintracerebral hemorrhageneovascularizationTWEAK
spellingShingle Daniel Romaus-Sanjurjo
Esteban López-Arias
Cristina Rodríguez
Pablo Hervella
Mariña Rodríguez-Arrizabalaga
Manuel Debasa-Mouce
Juan Manuel Pías-Peleteiro
Ramón Iglesias-Rey
Pablo Aguiar
Ángeles Almeida
José Castillo
Alberto Ouro
Tomás Sobrino
Blood Progenitor Cell Mobilization Driven by TWEAK Promotes Neovascularization and Reduces Brain Damage in a Rat Model of Intracerebral Hemorrhage
Antioxidants
endothelial progenitor cells
intracerebral hemorrhage
neovascularization
TWEAK
title Blood Progenitor Cell Mobilization Driven by TWEAK Promotes Neovascularization and Reduces Brain Damage in a Rat Model of Intracerebral Hemorrhage
title_full Blood Progenitor Cell Mobilization Driven by TWEAK Promotes Neovascularization and Reduces Brain Damage in a Rat Model of Intracerebral Hemorrhage
title_fullStr Blood Progenitor Cell Mobilization Driven by TWEAK Promotes Neovascularization and Reduces Brain Damage in a Rat Model of Intracerebral Hemorrhage
title_full_unstemmed Blood Progenitor Cell Mobilization Driven by TWEAK Promotes Neovascularization and Reduces Brain Damage in a Rat Model of Intracerebral Hemorrhage
title_short Blood Progenitor Cell Mobilization Driven by TWEAK Promotes Neovascularization and Reduces Brain Damage in a Rat Model of Intracerebral Hemorrhage
title_sort blood progenitor cell mobilization driven by tweak promotes neovascularization and reduces brain damage in a rat model of intracerebral hemorrhage
topic endothelial progenitor cells
intracerebral hemorrhage
neovascularization
TWEAK
url https://www.mdpi.com/2076-3921/14/5/601
work_keys_str_mv AT danielromaussanjurjo bloodprogenitorcellmobilizationdrivenbytweakpromotesneovascularizationandreducesbraindamageinaratmodelofintracerebralhemorrhage
AT estebanlopezarias bloodprogenitorcellmobilizationdrivenbytweakpromotesneovascularizationandreducesbraindamageinaratmodelofintracerebralhemorrhage
AT cristinarodriguez bloodprogenitorcellmobilizationdrivenbytweakpromotesneovascularizationandreducesbraindamageinaratmodelofintracerebralhemorrhage
AT pablohervella bloodprogenitorcellmobilizationdrivenbytweakpromotesneovascularizationandreducesbraindamageinaratmodelofintracerebralhemorrhage
AT marinarodriguezarrizabalaga bloodprogenitorcellmobilizationdrivenbytweakpromotesneovascularizationandreducesbraindamageinaratmodelofintracerebralhemorrhage
AT manueldebasamouce bloodprogenitorcellmobilizationdrivenbytweakpromotesneovascularizationandreducesbraindamageinaratmodelofintracerebralhemorrhage
AT juanmanuelpiaspeleteiro bloodprogenitorcellmobilizationdrivenbytweakpromotesneovascularizationandreducesbraindamageinaratmodelofintracerebralhemorrhage
AT ramoniglesiasrey bloodprogenitorcellmobilizationdrivenbytweakpromotesneovascularizationandreducesbraindamageinaratmodelofintracerebralhemorrhage
AT pabloaguiar bloodprogenitorcellmobilizationdrivenbytweakpromotesneovascularizationandreducesbraindamageinaratmodelofintracerebralhemorrhage
AT angelesalmeida bloodprogenitorcellmobilizationdrivenbytweakpromotesneovascularizationandreducesbraindamageinaratmodelofintracerebralhemorrhage
AT josecastillo bloodprogenitorcellmobilizationdrivenbytweakpromotesneovascularizationandreducesbraindamageinaratmodelofintracerebralhemorrhage
AT albertoouro bloodprogenitorcellmobilizationdrivenbytweakpromotesneovascularizationandreducesbraindamageinaratmodelofintracerebralhemorrhage
AT tomassobrino bloodprogenitorcellmobilizationdrivenbytweakpromotesneovascularizationandreducesbraindamageinaratmodelofintracerebralhemorrhage