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S100B promotes microglia M1 polarization and migration to aggravate cerebral ischemia
Aim and objective S100B has been found abundantly expressed in microglia during cerebral ischemia. However, S100B effects on phenotype changes and migration of microglia are unclear. Methods Real-time PCR of S100B, M1 and M2 markers were tested to characterize phenotypic changes in microglia in mice...
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| Published in: | Inflammation research 2018-12, Vol.67 (11-12), p.937-949 |
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| container_end_page | 949 |
| container_issue | 11-12 |
| container_start_page | 937 |
| container_title | Inflammation research |
| container_volume | 67 |
| creator | Zhou, Saijun Zhu, Weiqian Zhang, Yang Pan, Sipei Bao, Jianhong |
| description | Aim and objective
S100B has been found abundantly expressed in microglia during cerebral ischemia. However, S100B effects on phenotype changes and migration of microglia are unclear.
Methods
Real-time PCR of S100B, M1 and M2 markers were tested to characterize phenotypic changes in microglia in mice middle cerebral artery occlusion (MCAO) model. Migration assay and additional mechanism studies were performed to elucidate the role of NF-κB in S100B-mediated microglia M1/M2 phenotype change and migration. Finally, S100B treatment on MCAO models was performed to show the in vivo evidence.
Results
S100B was identified as an induced gene with its pattern in accordance with M1 markers in mice MCAO model. That S100B was promoted by M1 stimuli whereas inhibited by M2 stimuli further confirmed S100B a M1 marker. Moreover, S100B promotes microglia M1 polarization with enhanced migration ability and inhibits M2 polarization. Additionally, NF-κB is essential in S100B control in microglia M1/M2 polarization and migration. Furthermore, S100B aggravated cerebral ischemia in murine MCAO model and exacerbated the microglia M1 polarization and migration.
Conclusions
Our findings demonstrate that S100B promotes microglia M1 polarization to aggravate cerebral ischemia, and provide a better understanding on the therapeutic effects of S100B and/or its antagonist/neutralization antibody in stroke. |
| doi_str_mv | 10.1007/s00011-018-1187-y |
| format | article |
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S100B has been found abundantly expressed in microglia during cerebral ischemia. However, S100B effects on phenotype changes and migration of microglia are unclear.
Methods
Real-time PCR of S100B, M1 and M2 markers were tested to characterize phenotypic changes in microglia in mice middle cerebral artery occlusion (MCAO) model. Migration assay and additional mechanism studies were performed to elucidate the role of NF-κB in S100B-mediated microglia M1/M2 phenotype change and migration. Finally, S100B treatment on MCAO models was performed to show the in vivo evidence.
Results
S100B was identified as an induced gene with its pattern in accordance with M1 markers in mice MCAO model. That S100B was promoted by M1 stimuli whereas inhibited by M2 stimuli further confirmed S100B a M1 marker. Moreover, S100B promotes microglia M1 polarization with enhanced migration ability and inhibits M2 polarization. Additionally, NF-κB is essential in S100B control in microglia M1/M2 polarization and migration. Furthermore, S100B aggravated cerebral ischemia in murine MCAO model and exacerbated the microglia M1 polarization and migration.
Conclusions
Our findings demonstrate that S100B promotes microglia M1 polarization to aggravate cerebral ischemia, and provide a better understanding on the therapeutic effects of S100B and/or its antagonist/neutralization antibody in stroke.</description><identifier>ISSN: 1023-3830</identifier><identifier>EISSN: 1420-908X</identifier><identifier>DOI: 10.1007/s00011-018-1187-y</identifier><identifier>PMID: 30229393</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Allergology ; Animal models ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Cell Death ; Cell Movement ; Cell Polarity ; Cerebral blood flow ; Dermatology ; Immunology ; Infarction, Middle Cerebral Artery - pathology ; Ischemia ; Male ; Markers ; Mice ; Mice, Inbred C57BL ; Microglia ; Microglia - physiology ; Neurology ; Neurons ; Neutralization ; NF-κB protein ; Occlusion ; Original Research Paper ; Pharmacology/Toxicology ; Phenotypes ; Polarization ; Rheumatology ; S100 Calcium Binding Protein beta Subunit - physiology ; S100b protein ; Stimuli ; Stroke</subject><ispartof>Inflammation research, 2018-12, Vol.67 (11-12), p.937-949</ispartof><rights>Springer Nature Switzerland AG 2018</rights><rights>Inflammation Research is a copyright of Springer, (2018). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-a19cfe2eae83d3d30632671ccd845ee02e983c1c300774925f83f5d3f9b83f313</citedby><cites>FETCH-LOGICAL-c372t-a19cfe2eae83d3d30632671ccd845ee02e983c1c300774925f83f5d3f9b83f313</cites><orcidid>0000-0002-2760-7887</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30229393$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Saijun</creatorcontrib><creatorcontrib>Zhu, Weiqian</creatorcontrib><creatorcontrib>Zhang, Yang</creatorcontrib><creatorcontrib>Pan, Sipei</creatorcontrib><creatorcontrib>Bao, Jianhong</creatorcontrib><title>S100B promotes microglia M1 polarization and migration to aggravate cerebral ischemia</title><title>Inflammation research</title><addtitle>Inflamm. Res</addtitle><addtitle>Inflamm Res</addtitle><description>Aim and objective
S100B has been found abundantly expressed in microglia during cerebral ischemia. However, S100B effects on phenotype changes and migration of microglia are unclear.
Methods
Real-time PCR of S100B, M1 and M2 markers were tested to characterize phenotypic changes in microglia in mice middle cerebral artery occlusion (MCAO) model. Migration assay and additional mechanism studies were performed to elucidate the role of NF-κB in S100B-mediated microglia M1/M2 phenotype change and migration. Finally, S100B treatment on MCAO models was performed to show the in vivo evidence.
Results
S100B was identified as an induced gene with its pattern in accordance with M1 markers in mice MCAO model. That S100B was promoted by M1 stimuli whereas inhibited by M2 stimuli further confirmed S100B a M1 marker. Moreover, S100B promotes microglia M1 polarization with enhanced migration ability and inhibits M2 polarization. Additionally, NF-κB is essential in S100B control in microglia M1/M2 polarization and migration. Furthermore, S100B aggravated cerebral ischemia in murine MCAO model and exacerbated the microglia M1 polarization and migration.
Conclusions
Our findings demonstrate that S100B promotes microglia M1 polarization to aggravate cerebral ischemia, and provide a better understanding on the therapeutic effects of S100B and/or its antagonist/neutralization antibody in stroke.</description><subject>Allergology</subject><subject>Animal models</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Death</subject><subject>Cell Movement</subject><subject>Cell Polarity</subject><subject>Cerebral blood flow</subject><subject>Dermatology</subject><subject>Immunology</subject><subject>Infarction, Middle Cerebral Artery - pathology</subject><subject>Ischemia</subject><subject>Male</subject><subject>Markers</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microglia</subject><subject>Microglia - physiology</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Neutralization</subject><subject>NF-κB protein</subject><subject>Occlusion</subject><subject>Original Research Paper</subject><subject>Pharmacology/Toxicology</subject><subject>Phenotypes</subject><subject>Polarization</subject><subject>Rheumatology</subject><subject>S100 Calcium Binding Protein beta Subunit - physiology</subject><subject>S100b protein</subject><subject>Stimuli</subject><subject>Stroke</subject><issn>1023-3830</issn><issn>1420-908X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp1kE1LxDAQhoMo7rr6A7xIwYuXaibZtulRF79A8aAL3kI2ndYu_ViTVlh_vbN0VRAkh8wwz7wz8zJ2DPwcOE8uPOccIOSgQgCVhOsdNoap4GHK1esuxVzIUCrJR-zA-yXRSiixz0aSC5HKVI7Z_JmUroKVa-u2Qx_UpXVtUZUmeIRg1VbGlZ-mK9smME1G1cINWdcGpqDkw3QYWHS4cKYKSm_fsC7NIdvLTeXxaPtP2Pzm-mV2Fz483d7PLh9CKxPRhQZSm6NAg0pm9HgsRZyAtZmaRohcYKqkBSvp2GSaiihXMo8ymacLCiTICTsbdGn_9x59p2taAavKNNj2Xgug1iimcwk9_YMu2941tB1RXMVpBNFGEAaKXPDeYa5XrqyNW2vgeuO5HjzX5LneeK7X1HOyVe4XNWY_Hd8mEyAGwFOpKdD9jv5f9QtVQ4te</recordid><startdate>20181201</startdate><enddate>20181201</enddate><creator>Zhou, Saijun</creator><creator>Zhu, Weiqian</creator><creator>Zhang, Yang</creator><creator>Pan, Sipei</creator><creator>Bao, Jianhong</creator><general>Springer International Publishing</general><general>Springer Nature B.V</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>3V.</scope><scope>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-2760-7887</orcidid></search><sort><creationdate>20181201</creationdate><title>S100B promotes microglia M1 polarization and migration to aggravate cerebral ischemia</title><author>Zhou, Saijun ; Zhu, Weiqian ; Zhang, Yang ; Pan, Sipei ; Bao, Jianhong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-a19cfe2eae83d3d30632671ccd845ee02e983c1c300774925f83f5d3f9b83f313</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Allergology</topic><topic>Animal models</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Death</topic><topic>Cell Movement</topic><topic>Cell Polarity</topic><topic>Cerebral blood flow</topic><topic>Dermatology</topic><topic>Immunology</topic><topic>Infarction, Middle Cerebral Artery - pathology</topic><topic>Ischemia</topic><topic>Male</topic><topic>Markers</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Microglia</topic><topic>Microglia - physiology</topic><topic>Neurology</topic><topic>Neurons</topic><topic>Neutralization</topic><topic>NF-κB protein</topic><topic>Occlusion</topic><topic>Original Research Paper</topic><topic>Pharmacology/Toxicology</topic><topic>Phenotypes</topic><topic>Polarization</topic><topic>Rheumatology</topic><topic>S100 Calcium Binding Protein beta Subunit - physiology</topic><topic>S100b protein</topic><topic>Stimuli</topic><topic>Stroke</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Saijun</creatorcontrib><creatorcontrib>Zhu, Weiqian</creatorcontrib><creatorcontrib>Zhang, Yang</creatorcontrib><creatorcontrib>Pan, Sipei</creatorcontrib><creatorcontrib>Bao, Jianhong</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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)</collection><collection>ProQuest Central</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</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>PML(ProQuest Medical Library)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Inflammation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Saijun</au><au>Zhu, Weiqian</au><au>Zhang, Yang</au><au>Pan, Sipei</au><au>Bao, Jianhong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>S100B promotes microglia M1 polarization and migration to aggravate cerebral ischemia</atitle><jtitle>Inflammation research</jtitle><stitle>Inflamm. Res</stitle><addtitle>Inflamm Res</addtitle><date>2018-12-01</date><risdate>2018</risdate><volume>67</volume><issue>11-12</issue><spage>937</spage><epage>949</epage><pages>937-949</pages><issn>1023-3830</issn><eissn>1420-908X</eissn><abstract>Aim and objective
S100B has been found abundantly expressed in microglia during cerebral ischemia. However, S100B effects on phenotype changes and migration of microglia are unclear.
Methods
Real-time PCR of S100B, M1 and M2 markers were tested to characterize phenotypic changes in microglia in mice middle cerebral artery occlusion (MCAO) model. Migration assay and additional mechanism studies were performed to elucidate the role of NF-κB in S100B-mediated microglia M1/M2 phenotype change and migration. Finally, S100B treatment on MCAO models was performed to show the in vivo evidence.
Results
S100B was identified as an induced gene with its pattern in accordance with M1 markers in mice MCAO model. That S100B was promoted by M1 stimuli whereas inhibited by M2 stimuli further confirmed S100B a M1 marker. Moreover, S100B promotes microglia M1 polarization with enhanced migration ability and inhibits M2 polarization. Additionally, NF-κB is essential in S100B control in microglia M1/M2 polarization and migration. Furthermore, S100B aggravated cerebral ischemia in murine MCAO model and exacerbated the microglia M1 polarization and migration.
Conclusions
Our findings demonstrate that S100B promotes microglia M1 polarization to aggravate cerebral ischemia, and provide a better understanding on the therapeutic effects of S100B and/or its antagonist/neutralization antibody in stroke.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>30229393</pmid><doi>10.1007/s00011-018-1187-y</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-2760-7887</orcidid></addata></record> |
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| subjects | Allergology Animal models Animals Biomedical and Life Sciences Biomedicine Cell Death Cell Movement Cell Polarity Cerebral blood flow Dermatology Immunology Infarction, Middle Cerebral Artery - pathology Ischemia Male Markers Mice Mice, Inbred C57BL Microglia Microglia - physiology Neurology Neurons Neutralization NF-κB protein Occlusion Original Research Paper Pharmacology/Toxicology Phenotypes Polarization Rheumatology S100 Calcium Binding Protein beta Subunit - physiology S100b protein Stimuli Stroke |
| title | S100B promotes microglia M1 polarization and migration to aggravate cerebral ischemia |
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