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CCL21-induced calcium transients and proliferation in primary mouse astrocytes: CXCR3-dependent and independent responses
Abstract CCL21 is a homeostatic chemokine that is expressed constitutively in secondary lymph nodes and attracts immune cells via chemokine receptor CCR7. In the brain however, CCL21 is inducibly expressed in damaged neurons both in vitro and in vivo and has been shown to activate microglia in vitro...
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Published in: | Brain, behavior, and immunity behavior, and immunity, 2010-07, Vol.24 (5), p.768-775 |
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description | Abstract CCL21 is a homeostatic chemokine that is expressed constitutively in secondary lymph nodes and attracts immune cells via chemokine receptor CCR7. In the brain however, CCL21 is inducibly expressed in damaged neurons both in vitro and in vivo and has been shown to activate microglia in vitro , albeit not through CCR7 but through chemokine receptor CXCR3. Therefore, a role for CCL21 in CXCR3-mediated neuron-microglia signaling has been proposed. It is well established that human and mouse astrocytes, like microglia, express CXCR3. However, effects of CCL21 on astrocytes have not been investigated yet. In this study, we have examined the effects of CCL21 on calcium transients and proliferation in primary mouse astrocytes. We show that similar to CXCR3-ligand CXCL10, CCL21 (10−9 M and 10−8 M) induced calcium transients in astrocytes, which were mediated through CXCR3. However, in response to high concentrations of CCL21 (10−7 M) calcium transients persisted in CXCR3-deficient astrocytes, whereas CXCL10 did not have any effect in these cells. Furthermore, prolonged exposure to CXCL10 or CCL21 promoted proliferation of wild type astrocytes. Although CXCL10-induced proliferation was absent in CXCR3-deficient astrocytes, CCL21-induced proliferation of these cells did not significantly differ from wild type conditions. It is therefore suggested that primary mouse astrocytes express an additional (chemokine-) receptor, which is activated at high CCL21 concentrations. |
doi_str_mv | 10.1016/j.bbi.2009.04.007 |
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In the brain however, CCL21 is inducibly expressed in damaged neurons both in vitro and in vivo and has been shown to activate microglia in vitro , albeit not through CCR7 but through chemokine receptor CXCR3. Therefore, a role for CCL21 in CXCR3-mediated neuron-microglia signaling has been proposed. It is well established that human and mouse astrocytes, like microglia, express CXCR3. However, effects of CCL21 on astrocytes have not been investigated yet. In this study, we have examined the effects of CCL21 on calcium transients and proliferation in primary mouse astrocytes. We show that similar to CXCR3-ligand CXCL10, CCL21 (10−9 M and 10−8 M) induced calcium transients in astrocytes, which were mediated through CXCR3. However, in response to high concentrations of CCL21 (10−7 M) calcium transients persisted in CXCR3-deficient astrocytes, whereas CXCL10 did not have any effect in these cells. Furthermore, prolonged exposure to CXCL10 or CCL21 promoted proliferation of wild type astrocytes. Although CXCL10-induced proliferation was absent in CXCR3-deficient astrocytes, CCL21-induced proliferation of these cells did not significantly differ from wild type conditions. It is therefore suggested that primary mouse astrocytes express an additional (chemokine-) receptor, which is activated at high CCL21 concentrations.</description><identifier>ISSN: 0889-1591</identifier><identifier>EISSN: 1090-2139</identifier><identifier>DOI: 10.1016/j.bbi.2009.04.007</identifier><identifier>PMID: 19401230</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Allergy and Immunology ; Animals ; Astrocyte ; Astrocytes - cytology ; Astrocytes - metabolism ; Calcium ; Calcium - metabolism ; CCL21 ; Cell Proliferation - drug effects ; Cells, Cultured ; Chemokine ; Chemokine CCL21 - metabolism ; Chemokine CCL21 - pharmacology ; CXCL10 ; CXCR3 ; Flow Cytometry ; Mice ; Proliferation ; Psychiatry ; Receptors, CXCR3 - metabolism ; Reverse Transcriptase Polymerase Chain Reaction</subject><ispartof>Brain, behavior, and immunity, 2010-07, Vol.24 (5), p.768-775</ispartof><rights>Elsevier Inc.</rights><rights>2009 Elsevier Inc.</rights><rights>Copyright 2009 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c505t-8b9b01e73cbeb67f8407c246af50b4b121f3e78cc26c49517adae4139f5946743</citedby><cites>FETCH-LOGICAL-c505t-8b9b01e73cbeb67f8407c246af50b4b121f3e78cc26c49517adae4139f5946743</cites></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/19401230$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Weering, Hilmar R.J. van</creatorcontrib><creatorcontrib>Jong, Arthur P.H. de</creatorcontrib><creatorcontrib>Haas, Alexander H. de</creatorcontrib><creatorcontrib>Biber, Knut P.H</creatorcontrib><creatorcontrib>Boddeke, Hendrikus W.G.M</creatorcontrib><title>CCL21-induced calcium transients and proliferation in primary mouse astrocytes: CXCR3-dependent and independent responses</title><title>Brain, behavior, and immunity</title><addtitle>Brain Behav Immun</addtitle><description>Abstract CCL21 is a homeostatic chemokine that is expressed constitutively in secondary lymph nodes and attracts immune cells via chemokine receptor CCR7. In the brain however, CCL21 is inducibly expressed in damaged neurons both in vitro and in vivo and has been shown to activate microglia in vitro , albeit not through CCR7 but through chemokine receptor CXCR3. Therefore, a role for CCL21 in CXCR3-mediated neuron-microglia signaling has been proposed. It is well established that human and mouse astrocytes, like microglia, express CXCR3. However, effects of CCL21 on astrocytes have not been investigated yet. In this study, we have examined the effects of CCL21 on calcium transients and proliferation in primary mouse astrocytes. We show that similar to CXCR3-ligand CXCL10, CCL21 (10−9 M and 10−8 M) induced calcium transients in astrocytes, which were mediated through CXCR3. However, in response to high concentrations of CCL21 (10−7 M) calcium transients persisted in CXCR3-deficient astrocytes, whereas CXCL10 did not have any effect in these cells. Furthermore, prolonged exposure to CXCL10 or CCL21 promoted proliferation of wild type astrocytes. Although CXCL10-induced proliferation was absent in CXCR3-deficient astrocytes, CCL21-induced proliferation of these cells did not significantly differ from wild type conditions. It is therefore suggested that primary mouse astrocytes express an additional (chemokine-) receptor, which is activated at high CCL21 concentrations.</description><subject>Allergy and Immunology</subject><subject>Animals</subject><subject>Astrocyte</subject><subject>Astrocytes - cytology</subject><subject>Astrocytes - metabolism</subject><subject>Calcium</subject><subject>Calcium - metabolism</subject><subject>CCL21</subject><subject>Cell Proliferation - drug effects</subject><subject>Cells, Cultured</subject><subject>Chemokine</subject><subject>Chemokine CCL21 - metabolism</subject><subject>Chemokine CCL21 - pharmacology</subject><subject>CXCL10</subject><subject>CXCR3</subject><subject>Flow Cytometry</subject><subject>Mice</subject><subject>Proliferation</subject><subject>Psychiatry</subject><subject>Receptors, CXCR3 - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><issn>0889-1591</issn><issn>1090-2139</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNqFkl-L1DAUxYMo7rj6AXyRvvnUem-TtI2CIMU_CwPCquBbSNNbyNimY9IK8-03dQYFH9w8JCScc8i9v8vYc4QCAatXh6LrXFECqAJEAVA_YDsEBXmJXD1kO2galaNUeMWexHgAAMmxecyuUAnAksOOndp2X2LufL9a6jNrRuvWKVuC8dGRX2JmfJ8dwzy6gYJZ3Owz59ODm0w4ZdO8RspMXMJsTwvF11n7vb3leU9H8n3y_7an9D_3QPE4-0jxKXs0mDHSs8t5zb59eP-1_ZTvP3-8ad_tcytBLnnTqQ6Qam476qp6aATUthSVGSR0osMSB051Y21ZWaEk1qY3JFL9g1SiqgW_Zi_PuamInyvFRU8uWhpH4yn9XtdScahT4v1KnpZEuWXiWWnDHGOgQV8aohH0hkYfdEKjNzQahE5okufFJX3tJur_Oi4skuDNWUCpG78cBR1tQpCwuEB20f3s_hv_9h-3HZ13CegPOlE8zGvwqc0adSw16C_bbGyjkcYF0sb5HUqAtDo</recordid><startdate>20100701</startdate><enddate>20100701</enddate><creator>Weering, Hilmar R.J. van</creator><creator>Jong, Arthur P.H. de</creator><creator>Haas, Alexander H. de</creator><creator>Biber, Knut P.H</creator><creator>Boddeke, Hendrikus W.G.M</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>7QG</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope></search><sort><creationdate>20100701</creationdate><title>CCL21-induced calcium transients and proliferation in primary mouse astrocytes: CXCR3-dependent and independent responses</title><author>Weering, Hilmar R.J. van ; Jong, Arthur P.H. de ; Haas, Alexander H. de ; Biber, Knut P.H ; Boddeke, Hendrikus W.G.M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c505t-8b9b01e73cbeb67f8407c246af50b4b121f3e78cc26c49517adae4139f5946743</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Allergy and Immunology</topic><topic>Animals</topic><topic>Astrocyte</topic><topic>Astrocytes - cytology</topic><topic>Astrocytes - metabolism</topic><topic>Calcium</topic><topic>Calcium - metabolism</topic><topic>CCL21</topic><topic>Cell Proliferation - drug effects</topic><topic>Cells, Cultured</topic><topic>Chemokine</topic><topic>Chemokine CCL21 - metabolism</topic><topic>Chemokine CCL21 - pharmacology</topic><topic>CXCL10</topic><topic>CXCR3</topic><topic>Flow Cytometry</topic><topic>Mice</topic><topic>Proliferation</topic><topic>Psychiatry</topic><topic>Receptors, CXCR3 - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Weering, Hilmar R.J. van</creatorcontrib><creatorcontrib>Jong, Arthur P.H. de</creatorcontrib><creatorcontrib>Haas, Alexander H. de</creatorcontrib><creatorcontrib>Biber, Knut P.H</creatorcontrib><creatorcontrib>Boddeke, Hendrikus W.G.M</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>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Brain, behavior, and immunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Weering, Hilmar R.J. van</au><au>Jong, Arthur P.H. de</au><au>Haas, Alexander H. de</au><au>Biber, Knut P.H</au><au>Boddeke, Hendrikus W.G.M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CCL21-induced calcium transients and proliferation in primary mouse astrocytes: CXCR3-dependent and independent responses</atitle><jtitle>Brain, behavior, and immunity</jtitle><addtitle>Brain Behav Immun</addtitle><date>2010-07-01</date><risdate>2010</risdate><volume>24</volume><issue>5</issue><spage>768</spage><epage>775</epage><pages>768-775</pages><issn>0889-1591</issn><eissn>1090-2139</eissn><abstract>Abstract CCL21 is a homeostatic chemokine that is expressed constitutively in secondary lymph nodes and attracts immune cells via chemokine receptor CCR7. In the brain however, CCL21 is inducibly expressed in damaged neurons both in vitro and in vivo and has been shown to activate microglia in vitro , albeit not through CCR7 but through chemokine receptor CXCR3. Therefore, a role for CCL21 in CXCR3-mediated neuron-microglia signaling has been proposed. It is well established that human and mouse astrocytes, like microglia, express CXCR3. However, effects of CCL21 on astrocytes have not been investigated yet. In this study, we have examined the effects of CCL21 on calcium transients and proliferation in primary mouse astrocytes. We show that similar to CXCR3-ligand CXCL10, CCL21 (10−9 M and 10−8 M) induced calcium transients in astrocytes, which were mediated through CXCR3. However, in response to high concentrations of CCL21 (10−7 M) calcium transients persisted in CXCR3-deficient astrocytes, whereas CXCL10 did not have any effect in these cells. Furthermore, prolonged exposure to CXCL10 or CCL21 promoted proliferation of wild type astrocytes. Although CXCL10-induced proliferation was absent in CXCR3-deficient astrocytes, CCL21-induced proliferation of these cells did not significantly differ from wild type conditions. It is therefore suggested that primary mouse astrocytes express an additional (chemokine-) receptor, which is activated at high CCL21 concentrations.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>19401230</pmid><doi>10.1016/j.bbi.2009.04.007</doi><tpages>8</tpages></addata></record> |
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subjects | Allergy and Immunology Animals Astrocyte Astrocytes - cytology Astrocytes - metabolism Calcium Calcium - metabolism CCL21 Cell Proliferation - drug effects Cells, Cultured Chemokine Chemokine CCL21 - metabolism Chemokine CCL21 - pharmacology CXCL10 CXCR3 Flow Cytometry Mice Proliferation Psychiatry Receptors, CXCR3 - metabolism Reverse Transcriptase Polymerase Chain Reaction |
title | CCL21-induced calcium transients and proliferation in primary mouse astrocytes: CXCR3-dependent and independent responses |
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