Inhibition of endogenous blood glutamate oxaloacetate transaminase enhances the ischemic damage

Glutamate oxaloacetate transaminase 1 (GOT1) enzyme plays a critical role in the cell metabolism by participating in the carbohydrate and amino acid metabolism. In ischemic stroke, we have demonstrated that recombinant GOT1 acts as a novel neuroprotective treatment against the excess of extracellula...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Translational research : the journal of laboratory and clinical medicine 2021-04, Vol.230, p.68-81
Hauptverfasser: Dopico-López, Antonio, Pérez-Mato, María, da Silva-Candal, Andrés, Iglesias-Rey, Ramón, Rabinkov, Aharon, Bugallo-Casal, Ana, Sobrino, Tomás, Mirelman, David, Castillo, José, Campos, Francisco
Format: Artikel
Sprache:eng
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 81
container_issue
container_start_page 68
container_title Translational research : the journal of laboratory and clinical medicine
container_volume 230
creator Dopico-López, Antonio
Pérez-Mato, María
da Silva-Candal, Andrés
Iglesias-Rey, Ramón
Rabinkov, Aharon
Bugallo-Casal, Ana
Sobrino, Tomás
Mirelman, David
Castillo, José
Campos, Francisco
description Glutamate oxaloacetate transaminase 1 (GOT1) enzyme plays a critical role in the cell metabolism by participating in the carbohydrate and amino acid metabolism. In ischemic stroke, we have demonstrated that recombinant GOT1 acts as a novel neuroprotective treatment against the excess of extracellular glutamate that accumulates in the brain following ischemic stroke. In this study, we investigated the inhibitory effect of GOT1 on brain metabolism and on the ischemic damage in a rat model of ischemic stroke by means of a specific antibody developed against this enzyme. Inhibition of GOT1 caused higher brain glutamate and lactate levels and this response was associated with larger ischemic lesion. This study represents the first demonstration that the inhibition of the blood GOT1 activity leads to more severe ischemic damage and poorer outcome and supports the protective role of GOT1 against ischemic insults.
doi_str_mv 10.1016/j.trsl.2020.10.004
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2456856760</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S1931524420302450</els_id><sourcerecordid>2456856760</sourcerecordid><originalsourceid>FETCH-LOGICAL-c356t-9a2b195e7561cac4c4f3a147df438d23b6dca11a15fa801885c844a7e6ba57e43</originalsourceid><addsrcrecordid>eNp9kM1OGzEURi1UBDTtC7BAs-xmUnv8M47EBiFoI0XqpqytO_adxNHMONgOgrfHo0CXXdm-Ot8n30PINaNLRpn6uV_mmIZlQ5t5sKRUnJErpltdM83ol3JfcVbLRohL8jWlfQHUiooLcsk54w3V7RUx62nnO599mKrQVzi5sMUpHFPVDSG4ajscM4yQsQqvMASwmOdHjjAlGP0ECUtoB5PFVOUdVj7ZHY7eVq7EtviNnPcwJPz-cS7I0-PD3_vf9ebPr_X93aa2XKpcr6Dp2EpiKxWzYIUVPQcmWtcLrl3DO-UsMAZM9qAp01paLQS0qDqQLQq-ID9OvYcYno-YshnLT3AYYMKyjWmEVFqqVtGCNifUxpBSxN4coh8hvhlGzSzW7M0s1sxi51nxVkI3H_3HbkT3L_JpsgC3JwDLli8eo0nWY9HifESbjQv-f_3vOk2LcA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2456856760</pqid></control><display><type>article</type><title>Inhibition of endogenous blood glutamate oxaloacetate transaminase enhances the ischemic damage</title><source>Elsevier ScienceDirect Journals</source><creator>Dopico-López, Antonio ; Pérez-Mato, María ; da Silva-Candal, Andrés ; Iglesias-Rey, Ramón ; Rabinkov, Aharon ; Bugallo-Casal, Ana ; Sobrino, Tomás ; Mirelman, David ; Castillo, José ; Campos, Francisco</creator><creatorcontrib>Dopico-López, Antonio ; Pérez-Mato, María ; da Silva-Candal, Andrés ; Iglesias-Rey, Ramón ; Rabinkov, Aharon ; Bugallo-Casal, Ana ; Sobrino, Tomás ; Mirelman, David ; Castillo, José ; Campos, Francisco</creatorcontrib><description>Glutamate oxaloacetate transaminase 1 (GOT1) enzyme plays a critical role in the cell metabolism by participating in the carbohydrate and amino acid metabolism. In ischemic stroke, we have demonstrated that recombinant GOT1 acts as a novel neuroprotective treatment against the excess of extracellular glutamate that accumulates in the brain following ischemic stroke. In this study, we investigated the inhibitory effect of GOT1 on brain metabolism and on the ischemic damage in a rat model of ischemic stroke by means of a specific antibody developed against this enzyme. Inhibition of GOT1 caused higher brain glutamate and lactate levels and this response was associated with larger ischemic lesion. This study represents the first demonstration that the inhibition of the blood GOT1 activity leads to more severe ischemic damage and poorer outcome and supports the protective role of GOT1 against ischemic insults.</description><identifier>ISSN: 1931-5244</identifier><identifier>EISSN: 1878-1810</identifier><identifier>DOI: 10.1016/j.trsl.2020.10.004</identifier><identifier>PMID: 33132087</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><ispartof>Translational research : the journal of laboratory and clinical medicine, 2021-04, Vol.230, p.68-81</ispartof><rights>2020 Elsevier Inc.</rights><rights>Copyright © 2020 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c356t-9a2b195e7561cac4c4f3a147df438d23b6dca11a15fa801885c844a7e6ba57e43</citedby><cites>FETCH-LOGICAL-c356t-9a2b195e7561cac4c4f3a147df438d23b6dca11a15fa801885c844a7e6ba57e43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1931524420302450$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33132087$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dopico-López, Antonio</creatorcontrib><creatorcontrib>Pérez-Mato, María</creatorcontrib><creatorcontrib>da Silva-Candal, Andrés</creatorcontrib><creatorcontrib>Iglesias-Rey, Ramón</creatorcontrib><creatorcontrib>Rabinkov, Aharon</creatorcontrib><creatorcontrib>Bugallo-Casal, Ana</creatorcontrib><creatorcontrib>Sobrino, Tomás</creatorcontrib><creatorcontrib>Mirelman, David</creatorcontrib><creatorcontrib>Castillo, José</creatorcontrib><creatorcontrib>Campos, Francisco</creatorcontrib><title>Inhibition of endogenous blood glutamate oxaloacetate transaminase enhances the ischemic damage</title><title>Translational research : the journal of laboratory and clinical medicine</title><addtitle>Transl Res</addtitle><description>Glutamate oxaloacetate transaminase 1 (GOT1) enzyme plays a critical role in the cell metabolism by participating in the carbohydrate and amino acid metabolism. In ischemic stroke, we have demonstrated that recombinant GOT1 acts as a novel neuroprotective treatment against the excess of extracellular glutamate that accumulates in the brain following ischemic stroke. In this study, we investigated the inhibitory effect of GOT1 on brain metabolism and on the ischemic damage in a rat model of ischemic stroke by means of a specific antibody developed against this enzyme. Inhibition of GOT1 caused higher brain glutamate and lactate levels and this response was associated with larger ischemic lesion. This study represents the first demonstration that the inhibition of the blood GOT1 activity leads to more severe ischemic damage and poorer outcome and supports the protective role of GOT1 against ischemic insults.</description><issn>1931-5244</issn><issn>1878-1810</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp9kM1OGzEURi1UBDTtC7BAs-xmUnv8M47EBiFoI0XqpqytO_adxNHMONgOgrfHo0CXXdm-Ot8n30PINaNLRpn6uV_mmIZlQ5t5sKRUnJErpltdM83ol3JfcVbLRohL8jWlfQHUiooLcsk54w3V7RUx62nnO599mKrQVzi5sMUpHFPVDSG4ajscM4yQsQqvMASwmOdHjjAlGP0ECUtoB5PFVOUdVj7ZHY7eVq7EtviNnPcwJPz-cS7I0-PD3_vf9ebPr_X93aa2XKpcr6Dp2EpiKxWzYIUVPQcmWtcLrl3DO-UsMAZM9qAp01paLQS0qDqQLQq-ID9OvYcYno-YshnLT3AYYMKyjWmEVFqqVtGCNifUxpBSxN4coh8hvhlGzSzW7M0s1sxi51nxVkI3H_3HbkT3L_JpsgC3JwDLli8eo0nWY9HifESbjQv-f_3vOk2LcA</recordid><startdate>202104</startdate><enddate>202104</enddate><creator>Dopico-López, Antonio</creator><creator>Pérez-Mato, María</creator><creator>da Silva-Candal, Andrés</creator><creator>Iglesias-Rey, Ramón</creator><creator>Rabinkov, Aharon</creator><creator>Bugallo-Casal, Ana</creator><creator>Sobrino, Tomás</creator><creator>Mirelman, David</creator><creator>Castillo, José</creator><creator>Campos, Francisco</creator><general>Elsevier Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>202104</creationdate><title>Inhibition of endogenous blood glutamate oxaloacetate transaminase enhances the ischemic damage</title><author>Dopico-López, Antonio ; Pérez-Mato, María ; da Silva-Candal, Andrés ; Iglesias-Rey, Ramón ; Rabinkov, Aharon ; Bugallo-Casal, Ana ; Sobrino, Tomás ; Mirelman, David ; Castillo, José ; Campos, Francisco</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-9a2b195e7561cac4c4f3a147df438d23b6dca11a15fa801885c844a7e6ba57e43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dopico-López, Antonio</creatorcontrib><creatorcontrib>Pérez-Mato, María</creatorcontrib><creatorcontrib>da Silva-Candal, Andrés</creatorcontrib><creatorcontrib>Iglesias-Rey, Ramón</creatorcontrib><creatorcontrib>Rabinkov, Aharon</creatorcontrib><creatorcontrib>Bugallo-Casal, Ana</creatorcontrib><creatorcontrib>Sobrino, Tomás</creatorcontrib><creatorcontrib>Mirelman, David</creatorcontrib><creatorcontrib>Castillo, José</creatorcontrib><creatorcontrib>Campos, Francisco</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Translational research : the journal of laboratory and clinical medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dopico-López, Antonio</au><au>Pérez-Mato, María</au><au>da Silva-Candal, Andrés</au><au>Iglesias-Rey, Ramón</au><au>Rabinkov, Aharon</au><au>Bugallo-Casal, Ana</au><au>Sobrino, Tomás</au><au>Mirelman, David</au><au>Castillo, José</au><au>Campos, Francisco</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of endogenous blood glutamate oxaloacetate transaminase enhances the ischemic damage</atitle><jtitle>Translational research : the journal of laboratory and clinical medicine</jtitle><addtitle>Transl Res</addtitle><date>2021-04</date><risdate>2021</risdate><volume>230</volume><spage>68</spage><epage>81</epage><pages>68-81</pages><issn>1931-5244</issn><eissn>1878-1810</eissn><abstract>Glutamate oxaloacetate transaminase 1 (GOT1) enzyme plays a critical role in the cell metabolism by participating in the carbohydrate and amino acid metabolism. In ischemic stroke, we have demonstrated that recombinant GOT1 acts as a novel neuroprotective treatment against the excess of extracellular glutamate that accumulates in the brain following ischemic stroke. In this study, we investigated the inhibitory effect of GOT1 on brain metabolism and on the ischemic damage in a rat model of ischemic stroke by means of a specific antibody developed against this enzyme. Inhibition of GOT1 caused higher brain glutamate and lactate levels and this response was associated with larger ischemic lesion. This study represents the first demonstration that the inhibition of the blood GOT1 activity leads to more severe ischemic damage and poorer outcome and supports the protective role of GOT1 against ischemic insults.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>33132087</pmid><doi>10.1016/j.trsl.2020.10.004</doi><tpages>14</tpages></addata></record>
fulltext fulltext
identifier ISSN: 1931-5244
ispartof Translational research : the journal of laboratory and clinical medicine, 2021-04, Vol.230, p.68-81
issn 1931-5244
1878-1810
language eng
recordid cdi_proquest_miscellaneous_2456856760
source Elsevier ScienceDirect Journals
title Inhibition of endogenous blood glutamate oxaloacetate transaminase enhances the ischemic damage
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-26T07%3A56%3A21IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Inhibition%20of%20endogenous%20blood%20glutamate%20oxaloacetate%20transaminase%20enhances%20the%20ischemic%20damage&rft.jtitle=Translational%20research%20:%20the%20journal%20of%20laboratory%20and%20clinical%20medicine&rft.au=Dopico-L%C3%B3pez,%20Antonio&rft.date=2021-04&rft.volume=230&rft.spage=68&rft.epage=81&rft.pages=68-81&rft.issn=1931-5244&rft.eissn=1878-1810&rft_id=info:doi/10.1016/j.trsl.2020.10.004&rft_dat=%3Cproquest_cross%3E2456856760%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2456856760&rft_id=info:pmid/33132087&rft_els_id=S1931524420302450&rfr_iscdi=true