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HX600, a synthetic agonist for RXR-Nurr1 heterodimer complex, prevents ischemia-induced neuronal damage
•HX600 alleviates ischemia induced deficits in a mouse model of ischemic stroke.•HX600 treatment protects neurons from inflammation induced death in vitro.•HX600 treated microglia show reduced inflammatory activation in vitro and in vivo.•HX600 normalizes ischemia induced changes in fatty acid metab...
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Published in: | Brain, behavior, and immunity behavior, and immunity, 2018-10, Vol.73, p.670-681 |
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creator | Loppi, S. Kolosowska, N. Kärkkäinen, O. Korhonen, P. Huuskonen, M. Grubman, A. Dhungana, H. Wojciechowski, S. Pomeshchik, Y. Giordano, M. Kagechika, H. White, A. Auriola, S. Koistinaho, J. Landreth, G. Hanhineva, K. Kanninen, K. Malm, T. |
description | •HX600 alleviates ischemia induced deficits in a mouse model of ischemic stroke.•HX600 treatment protects neurons from inflammation induced death in vitro.•HX600 treated microglia show reduced inflammatory activation in vitro and in vivo.•HX600 normalizes ischemia induced changes in fatty acid metabolism.
Ischemic stroke is amongst the leading causes of death and disabilities. The available treatments are suitable for only a fraction of patients and thus novel therapies are urgently needed. Blockage of one of the cerebral arteries leads to massive and persisting inflammatory reaction contributing to the nearby neuronal damage. Targeting the detrimental pathways of neuroinflammation has been suggested to be beneficial in conditions of ischemic stroke. Nuclear receptor 4A-family (NR4A) member Nurr1 has been shown to be a potent modulator of harmful inflammatory reactions, yet the role of Nurr1 in cerebral stroke remains unknown. Here we show for the first time that an agonist for the dimeric transcription factor Nurr1/retinoid X receptor (RXR), HX600, reduces microglia expressed proinflammatory mediators and prevents inflammation induced neuronal death in in vitro co-culture model of neurons and microglia. Importantly, HX600 was protective in a mouse model of permanent middle cerebral artery occlusion and alleviated the stroke induced motor deficits. Along with the anti-inflammatory capacity of HX600 in vitro, treatment of ischemic mice with HX600 reduced ischemia induced Iba-1, p38 and TREM2 immunoreactivities, protected endogenous microglia from ischemia induced death and prevented leukocyte infiltration. These anti-inflammatory functions were associated with reduced levels of brain lysophosphatidylcholines (lysoPCs) and acylcarnitines, metabolites related to proinflammatory events. These data demonstrate that HX600 driven Nurr1 activation is beneficial in ischemic stroke and propose that targeting Nurr1 is a novel candidate for conditions involving neuroinflammatory component. |
doi_str_mv | 10.1016/j.bbi.2018.07.021 |
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Ischemic stroke is amongst the leading causes of death and disabilities. The available treatments are suitable for only a fraction of patients and thus novel therapies are urgently needed. Blockage of one of the cerebral arteries leads to massive and persisting inflammatory reaction contributing to the nearby neuronal damage. Targeting the detrimental pathways of neuroinflammation has been suggested to be beneficial in conditions of ischemic stroke. Nuclear receptor 4A-family (NR4A) member Nurr1 has been shown to be a potent modulator of harmful inflammatory reactions, yet the role of Nurr1 in cerebral stroke remains unknown. Here we show for the first time that an agonist for the dimeric transcription factor Nurr1/retinoid X receptor (RXR), HX600, reduces microglia expressed proinflammatory mediators and prevents inflammation induced neuronal death in in vitro co-culture model of neurons and microglia. Importantly, HX600 was protective in a mouse model of permanent middle cerebral artery occlusion and alleviated the stroke induced motor deficits. Along with the anti-inflammatory capacity of HX600 in vitro, treatment of ischemic mice with HX600 reduced ischemia induced Iba-1, p38 and TREM2 immunoreactivities, protected endogenous microglia from ischemia induced death and prevented leukocyte infiltration. These anti-inflammatory functions were associated with reduced levels of brain lysophosphatidylcholines (lysoPCs) and acylcarnitines, metabolites related to proinflammatory events. These data demonstrate that HX600 driven Nurr1 activation is beneficial in ischemic stroke and propose that targeting Nurr1 is a novel candidate for conditions involving neuroinflammatory component.</description><identifier>ISSN: 0889-1591</identifier><identifier>EISSN: 1090-2139</identifier><identifier>DOI: 10.1016/j.bbi.2018.07.021</identifier><identifier>PMID: 30063972</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Animals ; Brain - metabolism ; Brain Ischemia - metabolism ; Brain Ischemia - physiopathology ; Dibenzazepines - pharmacology ; Disease Models, Animal ; Infarction, Middle Cerebral Artery - metabolism ; Inflammation - metabolism ; Membrane Glycoproteins - analysis ; Membrane Glycoproteins - metabolism ; Metabolic profiling ; Mice ; Mice, Inbred C57BL ; Microglia ; Microglia - metabolism ; Nerve Degeneration - prevention & control ; Neuroinflammation ; Neurons - metabolism ; Neuroprotective Agents - pharmacology ; Nuclear Receptor Subfamily 4, Group A, Member 2 - agonists ; Nuclear Receptor Subfamily 4, Group A, Member 2 - physiology ; Nuclear receptors ; Primary Cell Culture ; Receptors, Cytoplasmic and Nuclear - metabolism ; Receptors, Immunologic - analysis ; Receptors, Immunologic - metabolism ; Retinoid X Receptors - agonists ; Retinoid X Receptors - physiology ; Stroke ; Stroke - metabolism</subject><ispartof>Brain, behavior, and immunity, 2018-10, Vol.73, p.670-681</ispartof><rights>2018 Elsevier Inc.</rights><rights>Copyright © 2018 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c517t-cd5bbe2e2c22ea139d1e974bda03e1c822b664d71f279e567b26d7791ec62de3</citedby><cites>FETCH-LOGICAL-c517t-cd5bbe2e2c22ea139d1e974bda03e1c822b664d71f279e567b26d7791ec62de3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30063972$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Loppi, S.</creatorcontrib><creatorcontrib>Kolosowska, N.</creatorcontrib><creatorcontrib>Kärkkäinen, O.</creatorcontrib><creatorcontrib>Korhonen, P.</creatorcontrib><creatorcontrib>Huuskonen, M.</creatorcontrib><creatorcontrib>Grubman, A.</creatorcontrib><creatorcontrib>Dhungana, H.</creatorcontrib><creatorcontrib>Wojciechowski, S.</creatorcontrib><creatorcontrib>Pomeshchik, Y.</creatorcontrib><creatorcontrib>Giordano, M.</creatorcontrib><creatorcontrib>Kagechika, H.</creatorcontrib><creatorcontrib>White, A.</creatorcontrib><creatorcontrib>Auriola, S.</creatorcontrib><creatorcontrib>Koistinaho, J.</creatorcontrib><creatorcontrib>Landreth, G.</creatorcontrib><creatorcontrib>Hanhineva, K.</creatorcontrib><creatorcontrib>Kanninen, K.</creatorcontrib><creatorcontrib>Malm, T.</creatorcontrib><title>HX600, a synthetic agonist for RXR-Nurr1 heterodimer complex, prevents ischemia-induced neuronal damage</title><title>Brain, behavior, and immunity</title><addtitle>Brain Behav Immun</addtitle><description>•HX600 alleviates ischemia induced deficits in a mouse model of ischemic stroke.•HX600 treatment protects neurons from inflammation induced death in vitro.•HX600 treated microglia show reduced inflammatory activation in vitro and in vivo.•HX600 normalizes ischemia induced changes in fatty acid metabolism.
Ischemic stroke is amongst the leading causes of death and disabilities. The available treatments are suitable for only a fraction of patients and thus novel therapies are urgently needed. Blockage of one of the cerebral arteries leads to massive and persisting inflammatory reaction contributing to the nearby neuronal damage. Targeting the detrimental pathways of neuroinflammation has been suggested to be beneficial in conditions of ischemic stroke. Nuclear receptor 4A-family (NR4A) member Nurr1 has been shown to be a potent modulator of harmful inflammatory reactions, yet the role of Nurr1 in cerebral stroke remains unknown. Here we show for the first time that an agonist for the dimeric transcription factor Nurr1/retinoid X receptor (RXR), HX600, reduces microglia expressed proinflammatory mediators and prevents inflammation induced neuronal death in in vitro co-culture model of neurons and microglia. Importantly, HX600 was protective in a mouse model of permanent middle cerebral artery occlusion and alleviated the stroke induced motor deficits. Along with the anti-inflammatory capacity of HX600 in vitro, treatment of ischemic mice with HX600 reduced ischemia induced Iba-1, p38 and TREM2 immunoreactivities, protected endogenous microglia from ischemia induced death and prevented leukocyte infiltration. These anti-inflammatory functions were associated with reduced levels of brain lysophosphatidylcholines (lysoPCs) and acylcarnitines, metabolites related to proinflammatory events. These data demonstrate that HX600 driven Nurr1 activation is beneficial in ischemic stroke and propose that targeting Nurr1 is a novel candidate for conditions involving neuroinflammatory component.</description><subject>Animals</subject><subject>Brain - metabolism</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - physiopathology</subject><subject>Dibenzazepines - pharmacology</subject><subject>Disease Models, Animal</subject><subject>Infarction, Middle Cerebral Artery - metabolism</subject><subject>Inflammation - metabolism</subject><subject>Membrane Glycoproteins - analysis</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Metabolic profiling</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microglia</subject><subject>Microglia - metabolism</subject><subject>Nerve Degeneration - prevention & control</subject><subject>Neuroinflammation</subject><subject>Neurons - metabolism</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Nuclear Receptor Subfamily 4, Group A, Member 2 - agonists</subject><subject>Nuclear Receptor Subfamily 4, Group A, Member 2 - physiology</subject><subject>Nuclear receptors</subject><subject>Primary Cell Culture</subject><subject>Receptors, Cytoplasmic and Nuclear - metabolism</subject><subject>Receptors, Immunologic - analysis</subject><subject>Receptors, Immunologic - metabolism</subject><subject>Retinoid X Receptors - agonists</subject><subject>Retinoid X Receptors - physiology</subject><subject>Stroke</subject><subject>Stroke - metabolism</subject><issn>0889-1591</issn><issn>1090-2139</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp9kUFv1DAQhS0EosuWH8AF-cihSWecTZwICamqgCJVVKp66M1y7NldrxJ7sZMV_fe42lLBpac5zJs3M-9j7ANCiYDN-a7se1cKwLYEWYLAV2yB0EEhsOpeswW0bVdg3eEJe5fSDgDqCtu37KQCaKpOigXbXN03AGdc8_Tgpy1NznC9Cd6lia9D5Lf3t8XPOUbkuUcxWDdS5CaM-4F-n_F9pAP5KXGXzJZGpwvn7WzIck9zDF4P3OpRb-iUvVnrIdH7p7pkd9--3l1eFdc3339cXlwXpkY5FcbWfU-ChBGCdP7CInVy1VsNFaFpheibZmUlroXsqG5kLxorZYdkGmGpWrIvR9v93I9kTb4t6kHtoxt1fFBBO_V_x7ut2oSDautVJXM8S_bpySCGXzOlSY35NRoG7SnMSQlosa4RRJuleJSaGFKKtH5eg6Ae-aidynzUIx8FUmU-eebjv_c9T_wFkgWfjwLKIR0cRZWMI58TdZHMpGxwL9j_AZ8Moj4</recordid><startdate>20181001</startdate><enddate>20181001</enddate><creator>Loppi, S.</creator><creator>Kolosowska, N.</creator><creator>Kärkkäinen, O.</creator><creator>Korhonen, P.</creator><creator>Huuskonen, M.</creator><creator>Grubman, A.</creator><creator>Dhungana, H.</creator><creator>Wojciechowski, S.</creator><creator>Pomeshchik, Y.</creator><creator>Giordano, M.</creator><creator>Kagechika, H.</creator><creator>White, A.</creator><creator>Auriola, S.</creator><creator>Koistinaho, J.</creator><creator>Landreth, G.</creator><creator>Hanhineva, K.</creator><creator>Kanninen, K.</creator><creator>Malm, T.</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20181001</creationdate><title>HX600, a synthetic agonist for RXR-Nurr1 heterodimer complex, prevents ischemia-induced neuronal damage</title><author>Loppi, S. ; Kolosowska, N. ; Kärkkäinen, O. ; Korhonen, P. ; Huuskonen, M. ; Grubman, A. ; Dhungana, H. ; Wojciechowski, S. ; Pomeshchik, Y. ; Giordano, M. ; Kagechika, H. ; White, A. ; Auriola, S. ; Koistinaho, J. ; Landreth, G. ; Hanhineva, K. ; Kanninen, K. ; Malm, T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c517t-cd5bbe2e2c22ea139d1e974bda03e1c822b664d71f279e567b26d7791ec62de3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Brain - metabolism</topic><topic>Brain Ischemia - metabolism</topic><topic>Brain Ischemia - physiopathology</topic><topic>Dibenzazepines - pharmacology</topic><topic>Disease Models, Animal</topic><topic>Infarction, Middle Cerebral Artery - metabolism</topic><topic>Inflammation - metabolism</topic><topic>Membrane Glycoproteins - analysis</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>Metabolic profiling</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Microglia</topic><topic>Microglia - metabolism</topic><topic>Nerve Degeneration - prevention & control</topic><topic>Neuroinflammation</topic><topic>Neurons - metabolism</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Nuclear Receptor Subfamily 4, Group A, Member 2 - agonists</topic><topic>Nuclear Receptor Subfamily 4, Group A, Member 2 - physiology</topic><topic>Nuclear receptors</topic><topic>Primary Cell Culture</topic><topic>Receptors, Cytoplasmic and Nuclear - metabolism</topic><topic>Receptors, Immunologic - analysis</topic><topic>Receptors, Immunologic - metabolism</topic><topic>Retinoid X Receptors - agonists</topic><topic>Retinoid X Receptors - physiology</topic><topic>Stroke</topic><topic>Stroke - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Loppi, S.</creatorcontrib><creatorcontrib>Kolosowska, N.</creatorcontrib><creatorcontrib>Kärkkäinen, O.</creatorcontrib><creatorcontrib>Korhonen, P.</creatorcontrib><creatorcontrib>Huuskonen, M.</creatorcontrib><creatorcontrib>Grubman, A.</creatorcontrib><creatorcontrib>Dhungana, H.</creatorcontrib><creatorcontrib>Wojciechowski, S.</creatorcontrib><creatorcontrib>Pomeshchik, Y.</creatorcontrib><creatorcontrib>Giordano, M.</creatorcontrib><creatorcontrib>Kagechika, H.</creatorcontrib><creatorcontrib>White, A.</creatorcontrib><creatorcontrib>Auriola, S.</creatorcontrib><creatorcontrib>Koistinaho, J.</creatorcontrib><creatorcontrib>Landreth, G.</creatorcontrib><creatorcontrib>Hanhineva, K.</creatorcontrib><creatorcontrib>Kanninen, K.</creatorcontrib><creatorcontrib>Malm, T.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Brain, behavior, and immunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Loppi, S.</au><au>Kolosowska, N.</au><au>Kärkkäinen, O.</au><au>Korhonen, P.</au><au>Huuskonen, M.</au><au>Grubman, A.</au><au>Dhungana, H.</au><au>Wojciechowski, S.</au><au>Pomeshchik, Y.</au><au>Giordano, M.</au><au>Kagechika, H.</au><au>White, A.</au><au>Auriola, S.</au><au>Koistinaho, J.</au><au>Landreth, G.</au><au>Hanhineva, K.</au><au>Kanninen, K.</au><au>Malm, T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HX600, a synthetic agonist for RXR-Nurr1 heterodimer complex, prevents ischemia-induced neuronal damage</atitle><jtitle>Brain, behavior, and immunity</jtitle><addtitle>Brain Behav Immun</addtitle><date>2018-10-01</date><risdate>2018</risdate><volume>73</volume><spage>670</spage><epage>681</epage><pages>670-681</pages><issn>0889-1591</issn><eissn>1090-2139</eissn><abstract>•HX600 alleviates ischemia induced deficits in a mouse model of ischemic stroke.•HX600 treatment protects neurons from inflammation induced death in vitro.•HX600 treated microglia show reduced inflammatory activation in vitro and in vivo.•HX600 normalizes ischemia induced changes in fatty acid metabolism.
Ischemic stroke is amongst the leading causes of death and disabilities. The available treatments are suitable for only a fraction of patients and thus novel therapies are urgently needed. Blockage of one of the cerebral arteries leads to massive and persisting inflammatory reaction contributing to the nearby neuronal damage. Targeting the detrimental pathways of neuroinflammation has been suggested to be beneficial in conditions of ischemic stroke. Nuclear receptor 4A-family (NR4A) member Nurr1 has been shown to be a potent modulator of harmful inflammatory reactions, yet the role of Nurr1 in cerebral stroke remains unknown. Here we show for the first time that an agonist for the dimeric transcription factor Nurr1/retinoid X receptor (RXR), HX600, reduces microglia expressed proinflammatory mediators and prevents inflammation induced neuronal death in in vitro co-culture model of neurons and microglia. Importantly, HX600 was protective in a mouse model of permanent middle cerebral artery occlusion and alleviated the stroke induced motor deficits. Along with the anti-inflammatory capacity of HX600 in vitro, treatment of ischemic mice with HX600 reduced ischemia induced Iba-1, p38 and TREM2 immunoreactivities, protected endogenous microglia from ischemia induced death and prevented leukocyte infiltration. These anti-inflammatory functions were associated with reduced levels of brain lysophosphatidylcholines (lysoPCs) and acylcarnitines, metabolites related to proinflammatory events. These data demonstrate that HX600 driven Nurr1 activation is beneficial in ischemic stroke and propose that targeting Nurr1 is a novel candidate for conditions involving neuroinflammatory component.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>30063972</pmid><doi>10.1016/j.bbi.2018.07.021</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Brain - metabolism Brain Ischemia - metabolism Brain Ischemia - physiopathology Dibenzazepines - pharmacology Disease Models, Animal Infarction, Middle Cerebral Artery - metabolism Inflammation - metabolism Membrane Glycoproteins - analysis Membrane Glycoproteins - metabolism Metabolic profiling Mice Mice, Inbred C57BL Microglia Microglia - metabolism Nerve Degeneration - prevention & control Neuroinflammation Neurons - metabolism Neuroprotective Agents - pharmacology Nuclear Receptor Subfamily 4, Group A, Member 2 - agonists Nuclear Receptor Subfamily 4, Group A, Member 2 - physiology Nuclear receptors Primary Cell Culture Receptors, Cytoplasmic and Nuclear - metabolism Receptors, Immunologic - analysis Receptors, Immunologic - metabolism Retinoid X Receptors - agonists Retinoid X Receptors - physiology Stroke Stroke - metabolism |
title | HX600, a synthetic agonist for RXR-Nurr1 heterodimer complex, prevents ischemia-induced neuronal damage |
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