Correlation of MR-Based Metabolomics and Molecular Profiling in the Tumor Microenvironment of Temozolomide-Treated Orthotopic GL261 Glioblastoma in Mice

The tumor microenvironment in glioblastoma (GB) is considered to be "cold", i.e., the fraction of cytotoxic T cells, for instance, is low. Instead, macrophages are the major immune cell population in GB, which stem either from tissue response (resident microglia) or recruitment of macropha...

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Autores: Zhao, Kai|||0009-0000-5186-2952, Calero-Perez, Pilar|||0000-0001-9370-3757, Bopp, Miriam H.A.|||0000-0003-1574-7572, Möschl, Vincent, Pagenstecher, Axel|||0000-0001-9627-6439, Mulero-Acevedo, Marta|||0000-0002-3600-8907, Vázquez, Mario, Barcia, Carlos|||0000-0003-0976-4245, Arús i Caraltó, Carles|||0000-0003-2510-2671, Nimsky, Christopher|||0000-0002-8216-9410, Rusch, Tillmann|||0009-0007-4848-5464, Bartsch, Joerg Walter.|||0000-0002-2773-3357, Candiota Silveira, Ana Paula|||0000-0002-1523-6505
Tipo de recurso: artículo
Fecha de publicación:2023
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:ddd.uab.cat:289015
Acceso en línea:https://ddd.uab.cat/record/289015
https://dx.doi.org/urn:doi:10.3390/ijms242417628
Access Level:acceso abierto
Palabra clave:MR spectroscopic imaging
PD-L1
Glioblastoma
Macrophages
Metalloproteases
Shedding
Temozolomide
Therapy
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spelling Correlation of MR-Based Metabolomics and Molecular Profiling in the Tumor Microenvironment of Temozolomide-Treated Orthotopic GL261 Glioblastoma in MiceZhao, Kai|||0009-0000-5186-2952Calero-Perez, Pilar|||0000-0001-9370-3757Bopp, Miriam H.A.|||0000-0003-1574-7572Möschl, VincentPagenstecher, Axel|||0000-0001-9627-6439Mulero-Acevedo, Marta|||0000-0002-3600-8907Vázquez, MarioBarcia, Carlos|||0000-0003-0976-4245Arús i Caraltó, Carles|||0000-0003-2510-2671Nimsky, Christopher|||0000-0002-8216-9410Rusch, Tillmann|||0009-0007-4848-5464Bartsch, Joerg Walter.|||0000-0002-2773-3357Candiota Silveira, Ana Paula|||0000-0002-1523-6505MR spectroscopic imagingPD-L1GlioblastomaMacrophagesMetalloproteasesSheddingTemozolomideTherapyThe tumor microenvironment in glioblastoma (GB) is considered to be "cold", i.e., the fraction of cytotoxic T cells, for instance, is low. Instead, macrophages are the major immune cell population in GB, which stem either from tissue response (resident microglia) or recruitment of macrophages from the periphery, thereby undergoing tumor-dependent "imprinting" mechanisms by which macrophages can adapt a tumor-supportive phenotype. In this regard, it is important to describe the nature of macrophages associated with GB, in particular under therapy conditions using the gold standard chemotherapy drug temozolomide (TMZ). Here, we explored the suitability of combining information from in vivo magnetic resonance spectroscopic (MRS) approaches (metabolomics) with in vitro molecular analyses to assess therapy response and characterize macrophage populations in mouse GB using an isogenic GL261 model. For macrophage profiling, expression levels of matrix metalloproteinases (MMPs) and A disintegrin and metalloproteinases (ADAMs) were determined, since their gene products affect macrophage-tumor cell communication by extensive cleavage of immunomodulatory membrane proteins, such as PD-L1. In tumor mice with an overall therapy response, expression of genes encoding the proteases ADAM8, ADAM10, and ADAM17 was increased and might contribute to the immunosuppressive phenotype of GB and immune cells. In tumors responding to therapy, expression levels of ADAM8 were upregulated by TMZ, and higher levels of PD-L1 were correlated significantly. Using a CRISPR/Cas9 knockout of ADAM8 in GL261 cells, we demonstrated that soluble PD-L1 (sPD-L1) is only generated in the presence of ADAM8. Moreover, primary macrophages from WT and ADAM8-deficient mice showed ADAM8-dependent release of sPD-L1, independent of the macrophage polarization state. Since ADAM8 expression is induced in responding tumors and PD-L1 shedding is likely to decrease the anti-tumor activities of T-cells, we conclude that immunotherapy resistance is caused, at least in part, by the increased presence of proteases, such as ADAM8. 22023-01-0120232023-01-01Articlehttp://purl.org/coar/resource_type/c_6501VoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttps://ddd.uab.cat/record/289015https://dx.doi.org/urn:doi:10.3390/ijms242417628reponame:Dipòsit Digital de Documents de la UABinstname:Universitat Autònoma de BarcelonaInglésengAgencia Estatal de Investigación https://doi.org/10.13039/501100011033 PID2021-128717OB-I00Ministerio de Sanidad y Consumo CB06/01/0010open accesshttp://purl.org/coar/access_right/c_abf2Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.https://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessoai:ddd.uab.cat:2890152026-06-06T12:50:31Z
dc.title.none.fl_str_mv Correlation of MR-Based Metabolomics and Molecular Profiling in the Tumor Microenvironment of Temozolomide-Treated Orthotopic GL261 Glioblastoma in Mice
title Correlation of MR-Based Metabolomics and Molecular Profiling in the Tumor Microenvironment of Temozolomide-Treated Orthotopic GL261 Glioblastoma in Mice
spellingShingle Correlation of MR-Based Metabolomics and Molecular Profiling in the Tumor Microenvironment of Temozolomide-Treated Orthotopic GL261 Glioblastoma in Mice
Zhao, Kai|||0009-0000-5186-2952
MR spectroscopic imaging
PD-L1
Glioblastoma
Macrophages
Metalloproteases
Shedding
Temozolomide
Therapy
title_short Correlation of MR-Based Metabolomics and Molecular Profiling in the Tumor Microenvironment of Temozolomide-Treated Orthotopic GL261 Glioblastoma in Mice
title_full Correlation of MR-Based Metabolomics and Molecular Profiling in the Tumor Microenvironment of Temozolomide-Treated Orthotopic GL261 Glioblastoma in Mice
title_fullStr Correlation of MR-Based Metabolomics and Molecular Profiling in the Tumor Microenvironment of Temozolomide-Treated Orthotopic GL261 Glioblastoma in Mice
title_full_unstemmed Correlation of MR-Based Metabolomics and Molecular Profiling in the Tumor Microenvironment of Temozolomide-Treated Orthotopic GL261 Glioblastoma in Mice
title_sort Correlation of MR-Based Metabolomics and Molecular Profiling in the Tumor Microenvironment of Temozolomide-Treated Orthotopic GL261 Glioblastoma in Mice
dc.creator.none.fl_str_mv Zhao, Kai|||0009-0000-5186-2952
Calero-Perez, Pilar|||0000-0001-9370-3757
Bopp, Miriam H.A.|||0000-0003-1574-7572
Möschl, Vincent
Pagenstecher, Axel|||0000-0001-9627-6439
Mulero-Acevedo, Marta|||0000-0002-3600-8907
Vázquez, Mario
Barcia, Carlos|||0000-0003-0976-4245
Arús i Caraltó, Carles|||0000-0003-2510-2671
Nimsky, Christopher|||0000-0002-8216-9410
Rusch, Tillmann|||0009-0007-4848-5464
Bartsch, Joerg Walter.|||0000-0002-2773-3357
Candiota Silveira, Ana Paula|||0000-0002-1523-6505
author Zhao, Kai|||0009-0000-5186-2952
author_facet Zhao, Kai|||0009-0000-5186-2952
Calero-Perez, Pilar|||0000-0001-9370-3757
Bopp, Miriam H.A.|||0000-0003-1574-7572
Möschl, Vincent
Pagenstecher, Axel|||0000-0001-9627-6439
Mulero-Acevedo, Marta|||0000-0002-3600-8907
Vázquez, Mario
Barcia, Carlos|||0000-0003-0976-4245
Arús i Caraltó, Carles|||0000-0003-2510-2671
Nimsky, Christopher|||0000-0002-8216-9410
Rusch, Tillmann|||0009-0007-4848-5464
Bartsch, Joerg Walter.|||0000-0002-2773-3357
Candiota Silveira, Ana Paula|||0000-0002-1523-6505
author_role author
author2 Calero-Perez, Pilar|||0000-0001-9370-3757
Bopp, Miriam H.A.|||0000-0003-1574-7572
Möschl, Vincent
Pagenstecher, Axel|||0000-0001-9627-6439
Mulero-Acevedo, Marta|||0000-0002-3600-8907
Vázquez, Mario
Barcia, Carlos|||0000-0003-0976-4245
Arús i Caraltó, Carles|||0000-0003-2510-2671
Nimsky, Christopher|||0000-0002-8216-9410
Rusch, Tillmann|||0009-0007-4848-5464
Bartsch, Joerg Walter.|||0000-0002-2773-3357
Candiota Silveira, Ana Paula|||0000-0002-1523-6505
author2_role author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv MR spectroscopic imaging
PD-L1
Glioblastoma
Macrophages
Metalloproteases
Shedding
Temozolomide
Therapy
topic MR spectroscopic imaging
PD-L1
Glioblastoma
Macrophages
Metalloproteases
Shedding
Temozolomide
Therapy
description The tumor microenvironment in glioblastoma (GB) is considered to be "cold", i.e., the fraction of cytotoxic T cells, for instance, is low. Instead, macrophages are the major immune cell population in GB, which stem either from tissue response (resident microglia) or recruitment of macrophages from the periphery, thereby undergoing tumor-dependent "imprinting" mechanisms by which macrophages can adapt a tumor-supportive phenotype. In this regard, it is important to describe the nature of macrophages associated with GB, in particular under therapy conditions using the gold standard chemotherapy drug temozolomide (TMZ). Here, we explored the suitability of combining information from in vivo magnetic resonance spectroscopic (MRS) approaches (metabolomics) with in vitro molecular analyses to assess therapy response and characterize macrophage populations in mouse GB using an isogenic GL261 model. For macrophage profiling, expression levels of matrix metalloproteinases (MMPs) and A disintegrin and metalloproteinases (ADAMs) were determined, since their gene products affect macrophage-tumor cell communication by extensive cleavage of immunomodulatory membrane proteins, such as PD-L1. In tumor mice with an overall therapy response, expression of genes encoding the proteases ADAM8, ADAM10, and ADAM17 was increased and might contribute to the immunosuppressive phenotype of GB and immune cells. In tumors responding to therapy, expression levels of ADAM8 were upregulated by TMZ, and higher levels of PD-L1 were correlated significantly. Using a CRISPR/Cas9 knockout of ADAM8 in GL261 cells, we demonstrated that soluble PD-L1 (sPD-L1) is only generated in the presence of ADAM8. Moreover, primary macrophages from WT and ADAM8-deficient mice showed ADAM8-dependent release of sPD-L1, independent of the macrophage polarization state. Since ADAM8 expression is induced in responding tumors and PD-L1 shedding is likely to decrease the anti-tumor activities of T-cells, we conclude that immunotherapy resistance is caused, at least in part, by the increased presence of proteases, such as ADAM8.
publishDate 2023
dc.date.none.fl_str_mv 2
2023-01-01
2023
2023-01-01
dc.type.none.fl_str_mv Article
http://purl.org/coar/resource_type/c_6501
VoR
http://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv https://ddd.uab.cat/record/289015
https://dx.doi.org/urn:doi:10.3390/ijms242417628
url https://ddd.uab.cat/record/289015
https://dx.doi.org/urn:doi:10.3390/ijms242417628
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.relation.none.fl_str_mv Agencia Estatal de Investigación https://doi.org/10.13039/501100011033 PID2021-128717OB-I00
Ministerio de Sanidad y Consumo CB06/01/0010
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
https://creativecommons.org/licenses/by/4.0/
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
https://creativecommons.org/licenses/by/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv reponame:Dipòsit Digital de Documents de la UAB
instname:Universitat Autònoma de Barcelona
instname_str Universitat Autònoma de Barcelona
reponame_str Dipòsit Digital de Documents de la UAB
collection Dipòsit Digital de Documents de la UAB
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