Plexin-B2 negatively regulates macrophage motility, Rac, and Cdc42 activation
Plexins are cell surface receptors widely studied in the nervous system, where they mediate migration and morphogenesis though the Rho family of small GTPases. More recently, plexins have been implicated in immune processes including cell-cell interaction, immune activation, migration, and cytokine...
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| creator | Roney, Kelly E O'Connor, Brian P Wen, Haitao Holl, Eda K Guthrie, Elizabeth H Davis, Beckley K Jones, Stephen W Jha, Sushmita Sharek, Lisa Garcia-Mata, Rafael Bear, James E Ting, Jenny P-Y |
| description | Plexins are cell surface receptors widely studied in the nervous system, where they mediate migration and morphogenesis though the Rho family of small GTPases. More recently, plexins have been implicated in immune processes including cell-cell interaction, immune activation, migration, and cytokine production. Plexin-B2 facilitates ligand induced cell guidance and migration in the nervous system, and induces cytoskeletal changes in overexpression assays through RhoGTPase. The function of Plexin-B2 in the immune system is unknown. This report shows that Plexin-B2 is highly expressed on cells of the innate immune system in the mouse, including macrophages, conventional dendritic cells, and plasmacytoid dendritic cells. However, Plexin-B2 does not appear to regulate the production of proinflammatory cytokines, phagocytosis of a variety of targets, or directional migration towards chemoattractants or extracellular matrix in mouse macrophages. Instead, Plxnb2(-/-) macrophages have greater cellular motility than wild type in the unstimulated state that is accompanied by more active, GTP-bound Rac and Cdc42. Additionally, Plxnb2(-/-) macrophages demonstrate faster in vitro wound closure activity. Studies have shown that a closely related family member, Plexin-B1, binds to active Rac and sequesters it from downstream signaling. The interaction of Plexin-B2 with Rac has only been previously confirmed in yeast and bacterial overexpression assays. The data presented here show that Plexin-B2 functions in mouse macrophages as a negative regulator of the GTPases Rac and Cdc42 and as a negative regulator of basal cell motility and wound healing. |
| doi_str_mv | 10.1371/journal.pone.0024795 |
| format | Article |
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More recently, plexins have been implicated in immune processes including cell-cell interaction, immune activation, migration, and cytokine production. Plexin-B2 facilitates ligand induced cell guidance and migration in the nervous system, and induces cytoskeletal changes in overexpression assays through RhoGTPase. The function of Plexin-B2 in the immune system is unknown. This report shows that Plexin-B2 is highly expressed on cells of the innate immune system in the mouse, including macrophages, conventional dendritic cells, and plasmacytoid dendritic cells. However, Plexin-B2 does not appear to regulate the production of proinflammatory cytokines, phagocytosis of a variety of targets, or directional migration towards chemoattractants or extracellular matrix in mouse macrophages. Instead, Plxnb2(-/-) macrophages have greater cellular motility than wild type in the unstimulated state that is accompanied by more active, GTP-bound Rac and Cdc42. Additionally, Plxnb2(-/-) macrophages demonstrate faster in vitro wound closure activity. Studies have shown that a closely related family member, Plexin-B1, binds to active Rac and sequesters it from downstream signaling. The interaction of Plexin-B2 with Rac has only been previously confirmed in yeast and bacterial overexpression assays. The data presented here show that Plexin-B2 functions in mouse macrophages as a negative regulator of the GTPases Rac and Cdc42 and as a negative regulator of basal cell motility and wound healing.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0024795</identifier><identifier>PMID: 21966369</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Antigen presenting cells ; Bacteria ; Biology ; Blotting, Western ; Bone Marrow Cells - metabolism ; cdc42 GTP-Binding Protein - metabolism ; Cdc42 protein ; Cell activation ; Cell adhesion & migration ; Cell Movement ; Cell surface ; Cell Transplantation - methods ; Cells, Cultured ; Chemotactic factors ; Cytokines ; Cytokines - metabolism ; Cytoskeleton ; Dendritic cells ; Developmental biology ; Drosophila ; E coli ; Extracellular matrix ; Female ; Flow Cytometry ; G proteins ; Guanosine triphosphate ; Humans ; Immune system ; Immunology ; Inflammation ; Innate immunity ; Insects ; Kinases ; Leukocyte Common Antigens - metabolism ; Leukocyte migration ; Ligands ; Liver - cytology ; Liver - embryology ; Liver - metabolism ; Macrophages ; Macrophages - cytology ; Macrophages - metabolism ; Male ; Mice ; Mice, Congenic ; Mice, Inbred C57BL ; Mice, Knockout ; Morphogenesis ; Motility ; Mutation ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Nervous system ; Phagocytosis ; Prostate cancer ; Protein Binding ; rac1 GTP-Binding Protein - metabolism ; Receptors ; Signaling ; Spleen - cytology ; Spleen - metabolism ; Wound healing ; Yeast</subject><ispartof>PloS one, 2011-09, Vol.6 (9), p.e24795-e24795</ispartof><rights>COPYRIGHT 2011 Public Library of Science</rights><rights>2011 Roney et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Roney et al. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c691t-dd55c04db544102aa07e274e195bac0e6266e593911afbd8679d58a324100ff3</citedby><cites>FETCH-LOGICAL-c691t-dd55c04db544102aa07e274e195bac0e6266e593911afbd8679d58a324100ff3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3179467/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3179467/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21966369$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Roney, Kelly E</creatorcontrib><creatorcontrib>O'Connor, Brian P</creatorcontrib><creatorcontrib>Wen, Haitao</creatorcontrib><creatorcontrib>Holl, Eda K</creatorcontrib><creatorcontrib>Guthrie, Elizabeth H</creatorcontrib><creatorcontrib>Davis, Beckley K</creatorcontrib><creatorcontrib>Jones, Stephen W</creatorcontrib><creatorcontrib>Jha, Sushmita</creatorcontrib><creatorcontrib>Sharek, Lisa</creatorcontrib><creatorcontrib>Garcia-Mata, Rafael</creatorcontrib><creatorcontrib>Bear, James E</creatorcontrib><creatorcontrib>Ting, Jenny P-Y</creatorcontrib><title>Plexin-B2 negatively regulates macrophage motility, Rac, and Cdc42 activation</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Plexins are cell surface receptors widely studied in the nervous system, where they mediate migration and morphogenesis though the Rho family of small GTPases. More recently, plexins have been implicated in immune processes including cell-cell interaction, immune activation, migration, and cytokine production. Plexin-B2 facilitates ligand induced cell guidance and migration in the nervous system, and induces cytoskeletal changes in overexpression assays through RhoGTPase. The function of Plexin-B2 in the immune system is unknown. This report shows that Plexin-B2 is highly expressed on cells of the innate immune system in the mouse, including macrophages, conventional dendritic cells, and plasmacytoid dendritic cells. However, Plexin-B2 does not appear to regulate the production of proinflammatory cytokines, phagocytosis of a variety of targets, or directional migration towards chemoattractants or extracellular matrix in mouse macrophages. Instead, Plxnb2(-/-) macrophages have greater cellular motility than wild type in the unstimulated state that is accompanied by more active, GTP-bound Rac and Cdc42. Additionally, Plxnb2(-/-) macrophages demonstrate faster in vitro wound closure activity. Studies have shown that a closely related family member, Plexin-B1, binds to active Rac and sequesters it from downstream signaling. The interaction of Plexin-B2 with Rac has only been previously confirmed in yeast and bacterial overexpression assays. 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metabolism</subject><subject>Leukocyte migration</subject><subject>Ligands</subject><subject>Liver - cytology</subject><subject>Liver - embryology</subject><subject>Liver - metabolism</subject><subject>Macrophages</subject><subject>Macrophages - cytology</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Congenic</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Morphogenesis</subject><subject>Motility</subject><subject>Mutation</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Nervous system</subject><subject>Phagocytosis</subject><subject>Prostate cancer</subject><subject>Protein Binding</subject><subject>rac1 GTP-Binding Protein - metabolism</subject><subject>Receptors</subject><subject>Signaling</subject><subject>Spleen - cytology</subject><subject>Spleen - metabolism</subject><subject>Wound healing</subject><subject>Yeast</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNku9r1DAYx4sobk7_A9GCoAi7M0nbpHkjzMMfg8lkDt-Gp8nTXo5cczbt2P335rxuXGUvJIGE9PP9PsnTb5K8pGROM0E_rPzQteDmG9_inBCWC1k8So6pzNiMM5I9PtgfJc9CWBFSZCXnT5MjRiXnGZfHyfcfDm9tO_vE0hYb6O0Num3aYTM46DGka9Cd3yyhwXTte-tsvz1Nr0CfptCadGF0zlLQURalvn2ePKnBBXwxrifJ9ZfP14tvs4vLr-eLs4uZ5pL2M2OKQpPcVEWeU8IAiEAmcqSyqEAT5IxzLGQmKYW6MiUX0hQlZCzSpK6zk-T13nbjfFBjI4KiGSlLWkQ6Eud7wnhYqU1n19BtlQer_h74rlHQ9VY7VFm8gaSilsaYHDWpasZB0FJrWhlOafT6OFYbqjUajW3fgZuYTr-0dqkafxOdhcy5iAbvRoPO_x4w9Gptg0bnoEU_BFVKznJWkF2pN_-QDz9upBqI97dt7WNZvfNUZ7ngpRBxRmr-ABWHwbXVMTS1jecTwfuJIDI93vYNDCGo859X_89e_pqybw_YJYLrl8G7YReYMAXzPRgjF0KH9X2PKVG7zN91Q-0yr8bMR9mrw_9zL7oLefYHh6v6sg</recordid><startdate>20110923</startdate><enddate>20110923</enddate><creator>Roney, Kelly E</creator><creator>O'Connor, Brian P</creator><creator>Wen, Haitao</creator><creator>Holl, Eda K</creator><creator>Guthrie, Elizabeth H</creator><creator>Davis, Beckley K</creator><creator>Jones, Stephen W</creator><creator>Jha, Sushmita</creator><creator>Sharek, Lisa</creator><creator>Garcia-Mata, Rafael</creator><creator>Bear, James E</creator><creator>Ting, Jenny P-Y</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20110923</creationdate><title>Plexin-B2 negatively regulates macrophage motility, Rac, and Cdc42 activation</title><author>Roney, Kelly E ; O'Connor, Brian P ; Wen, Haitao ; Holl, Eda K ; Guthrie, Elizabeth H ; Davis, Beckley K ; Jones, Stephen W ; Jha, Sushmita ; Sharek, Lisa ; Garcia-Mata, Rafael ; Bear, James E ; Ting, Jenny P-Y</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c691t-dd55c04db544102aa07e274e195bac0e6266e593911afbd8679d58a324100ff3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Antigen presenting cells</topic><topic>Bacteria</topic><topic>Biology</topic><topic>Blotting, Western</topic><topic>Bone Marrow Cells - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Roney, Kelly E</au><au>O'Connor, Brian P</au><au>Wen, Haitao</au><au>Holl, Eda K</au><au>Guthrie, Elizabeth H</au><au>Davis, Beckley K</au><au>Jones, Stephen W</au><au>Jha, Sushmita</au><au>Sharek, Lisa</au><au>Garcia-Mata, Rafael</au><au>Bear, James E</au><au>Ting, Jenny P-Y</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Plexin-B2 negatively regulates macrophage motility, Rac, and Cdc42 activation</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2011-09-23</date><risdate>2011</risdate><volume>6</volume><issue>9</issue><spage>e24795</spage><epage>e24795</epage><pages>e24795-e24795</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Plexins are cell surface receptors widely studied in the nervous system, where they mediate migration and morphogenesis though the Rho family of small GTPases. More recently, plexins have been implicated in immune processes including cell-cell interaction, immune activation, migration, and cytokine production. Plexin-B2 facilitates ligand induced cell guidance and migration in the nervous system, and induces cytoskeletal changes in overexpression assays through RhoGTPase. The function of Plexin-B2 in the immune system is unknown. This report shows that Plexin-B2 is highly expressed on cells of the innate immune system in the mouse, including macrophages, conventional dendritic cells, and plasmacytoid dendritic cells. However, Plexin-B2 does not appear to regulate the production of proinflammatory cytokines, phagocytosis of a variety of targets, or directional migration towards chemoattractants or extracellular matrix in mouse macrophages. Instead, Plxnb2(-/-) macrophages have greater cellular motility than wild type in the unstimulated state that is accompanied by more active, GTP-bound Rac and Cdc42. Additionally, Plxnb2(-/-) macrophages demonstrate faster in vitro wound closure activity. Studies have shown that a closely related family member, Plexin-B1, binds to active Rac and sequesters it from downstream signaling. The interaction of Plexin-B2 with Rac has only been previously confirmed in yeast and bacterial overexpression assays. The data presented here show that Plexin-B2 functions in mouse macrophages as a negative regulator of the GTPases Rac and Cdc42 and as a negative regulator of basal cell motility and wound healing.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>21966369</pmid><doi>10.1371/journal.pone.0024795</doi><tpages>e24795</tpages><oa>free_for_read</oa></addata></record> |
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| language | eng |
| recordid | cdi_plos_journals_1308815679 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Animals Antigen presenting cells Bacteria Biology Blotting, Western Bone Marrow Cells - metabolism cdc42 GTP-Binding Protein - metabolism Cdc42 protein Cell activation Cell adhesion & migration Cell Movement Cell surface Cell Transplantation - methods Cells, Cultured Chemotactic factors Cytokines Cytokines - metabolism Cytoskeleton Dendritic cells Developmental biology Drosophila E coli Extracellular matrix Female Flow Cytometry G proteins Guanosine triphosphate Humans Immune system Immunology Inflammation Innate immunity Insects Kinases Leukocyte Common Antigens - metabolism Leukocyte migration Ligands Liver - cytology Liver - embryology Liver - metabolism Macrophages Macrophages - cytology Macrophages - metabolism Male Mice Mice, Congenic Mice, Inbred C57BL Mice, Knockout Morphogenesis Motility Mutation Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Nervous system Phagocytosis Prostate cancer Protein Binding rac1 GTP-Binding Protein - metabolism Receptors Signaling Spleen - cytology Spleen - metabolism Wound healing Yeast |
| title | Plexin-B2 negatively regulates macrophage motility, Rac, and Cdc42 activation |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-08T16%3A28%3A27IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Plexin-B2%20negatively%20regulates%20macrophage%20motility,%20Rac,%20and%20Cdc42%20activation&rft.jtitle=PloS%20one&rft.au=Roney,%20Kelly%20E&rft.date=2011-09-23&rft.volume=6&rft.issue=9&rft.spage=e24795&rft.epage=e24795&rft.pages=e24795-e24795&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0024795&rft_dat=%3Cgale_plos_%3EA476877877%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1308815679&rft_id=info:pmid/21966369&rft_galeid=A476877877&rft_doaj_id=oai_doaj_org_article_3102917f9ddd4ec0bf26a718cc1bd611&rfr_iscdi=true |