FoxO1 Controls Redox Regulation and Cellular Physiology of BV-2 Microglial Cells
Microglia are brain-resident macrophage-like cells that play critical roles in diverse pathophysiological conditions, including development, neurogenesis, tissue damage, and pathogenic infection. Identifying molecular switches that govern the fate and function of microglia would be valuable for main...
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| Veröffentlicht in: | Inflammation 2023-04, Vol.46 (2), p.752-762 |
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| creator | Seong, Chaeeun Kim, Hyeon Ji Byun, Jin-Seok Kim, Yoonjung Kim, Do-Yeon |
| description | Microglia are brain-resident macrophage-like cells that play critical roles in diverse pathophysiological conditions, including development, neurogenesis, tissue damage, and pathogenic infection. Identifying molecular switches that govern the fate and function of microglia would be valuable for maintaining brain homeostasis. Forkhead box protein O1 (FoxO1) is the first identified gene in the FoxO family and serves as a potent transcriptional regulator that participates in development, apoptosis, metabolism, and stress response. It has been recently reported that FoxO1 expression is downregulated in human microglia with age, but the role of FoxO1 has not been characterized so far. In the present study, we investigated the molecular function of FoxO1 in microglia by utilizing BV-2 cells. By generating FoxO1-deficient BV-2 microglia through Crispr/Cas9 system, we analyzed the influence of FoxO1 on redox status, metabolism, and polarization of microglia. Our data clearly showed that FoxO1 deficiency suppressed oxidative stress and cell death. In addition, FoxO1 level could modulate metabolic status and polarizing potential of BV-2 microglia. FoxO1 might be a critical element for the regulation of microglial cell physiology and the maintenance of the brain homeostasis. |
| doi_str_mv | 10.1007/s10753-022-01771-5 |
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Identifying molecular switches that govern the fate and function of microglia would be valuable for maintaining brain homeostasis. Forkhead box protein O1 (FoxO1) is the first identified gene in the FoxO family and serves as a potent transcriptional regulator that participates in development, apoptosis, metabolism, and stress response. It has been recently reported that FoxO1 expression is downregulated in human microglia with age, but the role of FoxO1 has not been characterized so far. In the present study, we investigated the molecular function of FoxO1 in microglia by utilizing BV-2 cells. By generating FoxO1-deficient BV-2 microglia through Crispr/Cas9 system, we analyzed the influence of FoxO1 on redox status, metabolism, and polarization of microglia. Our data clearly showed that FoxO1 deficiency suppressed oxidative stress and cell death. In addition, FoxO1 level could modulate metabolic status and polarizing potential of BV-2 microglia. FoxO1 might be a critical element for the regulation of microglial cell physiology and the maintenance of the brain homeostasis.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-022-01771-5</identifier><identifier>PMID: 36515788</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Antioxidants - metabolism ; Apoptosis ; Biomedical and Life Sciences ; Biomedicine ; Brain - metabolism ; Cell death ; CRISPR ; Forkhead Box Protein O1 - metabolism ; Forkhead protein ; FOXO1 protein ; Homeostasis ; Humans ; Immunology ; Internal Medicine ; Macrophages ; Metabolism ; Mice ; Microglia ; Microglia - metabolism ; Microglial cells ; Neurogenesis ; Original Article ; Oxidation-Reduction ; Oxidative Stress ; Pathology ; Pharmacology/Toxicology ; Physiology ; Rheumatology</subject><ispartof>Inflammation, 2023-04, Vol.46 (2), p.752-762</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022. 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The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-debc93a05a4dcbd9806e25cd69750c4fb4d0249e0c99b469edaf89554c6707903</citedby><cites>FETCH-LOGICAL-c375t-debc93a05a4dcbd9806e25cd69750c4fb4d0249e0c99b469edaf89554c6707903</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10753-022-01771-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10753-022-01771-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36515788$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Seong, Chaeeun</creatorcontrib><creatorcontrib>Kim, Hyeon Ji</creatorcontrib><creatorcontrib>Byun, Jin-Seok</creatorcontrib><creatorcontrib>Kim, Yoonjung</creatorcontrib><creatorcontrib>Kim, Do-Yeon</creatorcontrib><title>FoxO1 Controls Redox Regulation and Cellular Physiology of BV-2 Microglial Cells</title><title>Inflammation</title><addtitle>Inflammation</addtitle><addtitle>Inflammation</addtitle><description>Microglia are brain-resident macrophage-like cells that play critical roles in diverse pathophysiological conditions, including development, neurogenesis, tissue damage, and pathogenic infection. 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Kim, Hyeon Ji ; Byun, Jin-Seok ; Kim, Yoonjung ; Kim, Do-Yeon</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-debc93a05a4dcbd9806e25cd69750c4fb4d0249e0c99b469edaf89554c6707903</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Animals</topic><topic>Antioxidants - metabolism</topic><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain - metabolism</topic><topic>Cell death</topic><topic>CRISPR</topic><topic>Forkhead Box Protein O1 - metabolism</topic><topic>Forkhead protein</topic><topic>FOXO1 protein</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Immunology</topic><topic>Internal Medicine</topic><topic>Macrophages</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Microglia</topic><topic>Microglia - metabolism</topic><topic>Microglial cells</topic><topic>Neurogenesis</topic><topic>Original Article</topic><topic>Oxidation-Reduction</topic><topic>Oxidative Stress</topic><topic>Pathology</topic><topic>Pharmacology/Toxicology</topic><topic>Physiology</topic><topic>Rheumatology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Seong, Chaeeun</creatorcontrib><creatorcontrib>Kim, Hyeon Ji</creatorcontrib><creatorcontrib>Byun, Jin-Seok</creatorcontrib><creatorcontrib>Kim, Yoonjung</creatorcontrib><creatorcontrib>Kim, Do-Yeon</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Seong, Chaeeun</au><au>Kim, Hyeon Ji</au><au>Byun, Jin-Seok</au><au>Kim, Yoonjung</au><au>Kim, Do-Yeon</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>FoxO1 Controls Redox Regulation and Cellular Physiology of BV-2 Microglial Cells</atitle><jtitle>Inflammation</jtitle><stitle>Inflammation</stitle><addtitle>Inflammation</addtitle><date>2023-04-01</date><risdate>2023</risdate><volume>46</volume><issue>2</issue><spage>752</spage><epage>762</epage><pages>752-762</pages><issn>0360-3997</issn><eissn>1573-2576</eissn><abstract>Microglia are brain-resident macrophage-like cells that play critical roles in diverse pathophysiological conditions, including development, neurogenesis, tissue damage, and pathogenic infection. Identifying molecular switches that govern the fate and function of microglia would be valuable for maintaining brain homeostasis. Forkhead box protein O1 (FoxO1) is the first identified gene in the FoxO family and serves as a potent transcriptional regulator that participates in development, apoptosis, metabolism, and stress response. It has been recently reported that FoxO1 expression is downregulated in human microglia with age, but the role of FoxO1 has not been characterized so far. In the present study, we investigated the molecular function of FoxO1 in microglia by utilizing BV-2 cells. By generating FoxO1-deficient BV-2 microglia through Crispr/Cas9 system, we analyzed the influence of FoxO1 on redox status, metabolism, and polarization of microglia. Our data clearly showed that FoxO1 deficiency suppressed oxidative stress and cell death. In addition, FoxO1 level could modulate metabolic status and polarizing potential of BV-2 microglia. 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| subjects | Animals Antioxidants - metabolism Apoptosis Biomedical and Life Sciences Biomedicine Brain - metabolism Cell death CRISPR Forkhead Box Protein O1 - metabolism Forkhead protein FOXO1 protein Homeostasis Humans Immunology Internal Medicine Macrophages Metabolism Mice Microglia Microglia - metabolism Microglial cells Neurogenesis Original Article Oxidation-Reduction Oxidative Stress Pathology Pharmacology/Toxicology Physiology Rheumatology |
| title | FoxO1 Controls Redox Regulation and Cellular Physiology of BV-2 Microglial Cells |
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