α2β1 integrin, GPVI receptor, and common FcRγ chain on mouse platelets mediate distinct responses to collagen in models of thrombosis
Platelets express the α2β1 integrin and the glycoprotein VI (GPVI)/FcRγ complex, both collagen receptors. Understanding platelet-collagen receptor function has been enhanced through use of genetically modified mouse models. Previous studies of GPVI/FcRγ-mediated collagen-induced platelet activation...
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| creator | Marjoram, Robin J Li, Zhengzhi He, Li Tollefsen, Douglas M Kunicki, Thomas J Dickeson, S Kent Santoro, Samuel A Zutter, Mary M |
| description | Platelets express the α2β1 integrin and the glycoprotein VI (GPVI)/FcRγ complex, both collagen receptors. Understanding platelet-collagen receptor function has been enhanced through use of genetically modified mouse models. Previous studies of GPVI/FcRγ-mediated collagen-induced platelet activation were perfomed with mice in which the FcRγ subunit was genetically deleted (FcRγ-/-) or the complex was depleted. The development of α2β1-/- and GPVI-/- mice permits side-by-side comparison to address contributions of these collagen receptors in vivo and in vitro.
To understand the different roles played by the α2β1 integrin, the GPVI receptor or FcRγ subunit in collagen-stimulated hemostasis and thrombosis, we compared α2β1-/-, FcRγ-/-, and GPVI-/- mice in models of endothelial injury and intravascular thrombosis in vivo and their platelets in collagen-stimulated activation in vitro. We demonstrate that both the α2β1 integrin and the GPVI receptor, but not the FcRγ subunit influence carotid artery occlusion in vivo. In contrast, the GPVI receptor and the FcRγ chain, but not the α2β1 integrin, play similar roles in intravascular thrombosis in response to soluble Type I collagen. FcRγ-/- platelets showed less attenuation of tyrosine phosphorylation of several proteins including RhoGDI when compared to GPVI-/- and wild type platelets. The difference between FcRγ-/- and GPVI-/- platelet phosphotyrosine levels correlated with the in vivo thrombosis findings.
Our data demonstrate that genetic deletion of GPVI receptor, FcRγ chain, or the α2β1 integrin changes the thrombotic potentials of these platelets to collagen dependent on the stimulus mechanism. The data suggest that the FcRγ chain may provide a dominant negative effect through modulating signaling pathways in platelets involving several tyrosine phosphorylated proteins such as RhoGDI. In addition, these findings suggest a more complex signaling network downstream of the platelet collagen receptors than previously appreciated. |
| doi_str_mv | 10.1371/journal.pone.0114035 |
| format | Article |
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To understand the different roles played by the α2β1 integrin, the GPVI receptor or FcRγ subunit in collagen-stimulated hemostasis and thrombosis, we compared α2β1-/-, FcRγ-/-, and GPVI-/- mice in models of endothelial injury and intravascular thrombosis in vivo and their platelets in collagen-stimulated activation in vitro. We demonstrate that both the α2β1 integrin and the GPVI receptor, but not the FcRγ subunit influence carotid artery occlusion in vivo. In contrast, the GPVI receptor and the FcRγ chain, but not the α2β1 integrin, play similar roles in intravascular thrombosis in response to soluble Type I collagen. FcRγ-/- platelets showed less attenuation of tyrosine phosphorylation of several proteins including RhoGDI when compared to GPVI-/- and wild type platelets. The difference between FcRγ-/- and GPVI-/- platelet phosphotyrosine levels correlated with the in vivo thrombosis findings.
Our data demonstrate that genetic deletion of GPVI receptor, FcRγ chain, or the α2β1 integrin changes the thrombotic potentials of these platelets to collagen dependent on the stimulus mechanism. The data suggest that the FcRγ chain may provide a dominant negative effect through modulating signaling pathways in platelets involving several tyrosine phosphorylated proteins such as RhoGDI. In addition, these findings suggest a more complex signaling network downstream of the platelet collagen receptors than previously appreciated.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0114035</identifier><identifier>PMID: 25415203</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Activation ; Animal models ; Animals ; Biology and Life Sciences ; Blood clots ; Blood platelets ; Blood Platelets - metabolism ; Carotid artery ; Cerebral blood flow ; Chains ; Collagen ; Collagen (type I) ; Collagen - adverse effects ; Collagen - pharmacology ; Disease Models, Animal ; Genetic modification ; Glycoprotein VI ; Glycoproteins ; Hemostasis ; Hemostatics ; Immunoglobulins ; Immunology ; Integrin alpha2beta1 - genetics ; Integrin alpha2beta1 - metabolism ; Ischemia ; Medicine ; Medicine and Health Sciences ; Mice ; Mice, Knockout ; Mutation ; Occlusion ; Pathology ; Phosphorylation ; Phosphotyrosine ; Platelet Activation - drug effects ; Platelet Activation - genetics ; Platelet Membrane Glycoproteins - genetics ; Platelet Membrane Glycoproteins - metabolism ; Platelets ; Proteins ; Rats ; Receptor mechanisms ; Receptors ; Receptors, IgG - genetics ; Receptors, IgG - metabolism ; Research and Analysis Methods ; Signaling ; Thromboembolism ; Thrombosis ; Thrombosis - chemically induced ; Thrombosis - genetics ; Thrombosis - metabolism ; Tyrosine</subject><ispartof>PloS one, 2014-11, Vol.9 (11), p.e114035</ispartof><rights>2014 Marjoram et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://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>2014 Marjoram et al 2014 Marjoram et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4415-7ef6ae9ee90cfa97c010cfa4942a79e0ec9724ffc189894715a6f26180adf1e43</citedby><cites>FETCH-LOGICAL-c4415-7ef6ae9ee90cfa97c010cfa4942a79e0ec9724ffc189894715a6f26180adf1e43</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/PMC4240667/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4240667/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,2096,2915,23847,27905,27906,53772,53774,79349,79350</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25415203$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Tseng, Ching-Ping</contributor><creatorcontrib>Marjoram, Robin J</creatorcontrib><creatorcontrib>Li, Zhengzhi</creatorcontrib><creatorcontrib>He, Li</creatorcontrib><creatorcontrib>Tollefsen, Douglas M</creatorcontrib><creatorcontrib>Kunicki, Thomas J</creatorcontrib><creatorcontrib>Dickeson, S Kent</creatorcontrib><creatorcontrib>Santoro, Samuel A</creatorcontrib><creatorcontrib>Zutter, Mary M</creatorcontrib><title>α2β1 integrin, GPVI receptor, and common FcRγ chain on mouse platelets mediate distinct responses to collagen in models of thrombosis</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Platelets express the α2β1 integrin and the glycoprotein VI (GPVI)/FcRγ complex, both collagen receptors. Understanding platelet-collagen receptor function has been enhanced through use of genetically modified mouse models. Previous studies of GPVI/FcRγ-mediated collagen-induced platelet activation were perfomed with mice in which the FcRγ subunit was genetically deleted (FcRγ-/-) or the complex was depleted. The development of α2β1-/- and GPVI-/- mice permits side-by-side comparison to address contributions of these collagen receptors in vivo and in vitro.
To understand the different roles played by the α2β1 integrin, the GPVI receptor or FcRγ subunit in collagen-stimulated hemostasis and thrombosis, we compared α2β1-/-, FcRγ-/-, and GPVI-/- mice in models of endothelial injury and intravascular thrombosis in vivo and their platelets in collagen-stimulated activation in vitro. We demonstrate that both the α2β1 integrin and the GPVI receptor, but not the FcRγ subunit influence carotid artery occlusion in vivo. In contrast, the GPVI receptor and the FcRγ chain, but not the α2β1 integrin, play similar roles in intravascular thrombosis in response to soluble Type I collagen. FcRγ-/- platelets showed less attenuation of tyrosine phosphorylation of several proteins including RhoGDI when compared to GPVI-/- and wild type platelets. The difference between FcRγ-/- and GPVI-/- platelet phosphotyrosine levels correlated with the in vivo thrombosis findings.
Our data demonstrate that genetic deletion of GPVI receptor, FcRγ chain, or the α2β1 integrin changes the thrombotic potentials of these platelets to collagen dependent on the stimulus mechanism. The data suggest that the FcRγ chain may provide a dominant negative effect through modulating signaling pathways in platelets involving several tyrosine phosphorylated proteins such as RhoGDI. In addition, these findings suggest a more complex signaling network downstream of the platelet collagen receptors than previously appreciated.</description><subject>Activation</subject><subject>Animal models</subject><subject>Animals</subject><subject>Biology and Life Sciences</subject><subject>Blood clots</subject><subject>Blood platelets</subject><subject>Blood Platelets - metabolism</subject><subject>Carotid artery</subject><subject>Cerebral blood flow</subject><subject>Chains</subject><subject>Collagen</subject><subject>Collagen (type I)</subject><subject>Collagen - adverse effects</subject><subject>Collagen - pharmacology</subject><subject>Disease Models, Animal</subject><subject>Genetic modification</subject><subject>Glycoprotein VI</subject><subject>Glycoproteins</subject><subject>Hemostasis</subject><subject>Hemostatics</subject><subject>Immunoglobulins</subject><subject>Immunology</subject><subject>Integrin alpha2beta1 - genetics</subject><subject>Integrin alpha2beta1 - metabolism</subject><subject>Ischemia</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Mutation</subject><subject>Occlusion</subject><subject>Pathology</subject><subject>Phosphorylation</subject><subject>Phosphotyrosine</subject><subject>Platelet Activation - drug effects</subject><subject>Platelet Activation - genetics</subject><subject>Platelet Membrane Glycoproteins - genetics</subject><subject>Platelet Membrane Glycoproteins - metabolism</subject><subject>Platelets</subject><subject>Proteins</subject><subject>Rats</subject><subject>Receptor mechanisms</subject><subject>Receptors</subject><subject>Receptors, IgG - genetics</subject><subject>Receptors, IgG - metabolism</subject><subject>Research and Analysis Methods</subject><subject>Signaling</subject><subject>Thromboembolism</subject><subject>Thrombosis</subject><subject>Thrombosis - chemically induced</subject><subject>Thrombosis - genetics</subject><subject>Thrombosis - metabolism</subject><subject>Tyrosine</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNp1ktFuFCEUhidGY2v1DYySeNtdgWEYuDExja2bNNEY9ZawzGGXDQMrsCa-ga-jvsc-k6w7bdoLrzgczv-dP-RvmucEz0nbk9ebuEtB-_k2BphjQhhuuwfNKZEtnXGK24d36pPmSc4bjLtWcP64OaEdI13tnzY_97_o_jdBLhRYJRfO0dXHrwuUwMC2xHSOdBiQieMYA7o0n_Z_kFlrF1C9jnGXAW29LuChZDTC4GqNBpeLC6ZUSK7mMmRUYmV4r1cQ6qaqHMBnFC0q6xTHZcwuP20eWe0zPJvOs-bL5bvPF-9n1x-uFhdvr2eGVc-zHizXIAEkNlbL3mByKJhkVPcSMBjZU2atIUIKyXrSaW4pJwLrwRJg7Vnz8sjd-pjV9IlZEU65oLQTvE4sjhND1Bu1TW7U6YeK2ql_jZhWSqfijAelMREcc6yp4UwwsVwyKaoh2murDSWV9WbatlvW_zEQStL-HvT-S3BrtYrfFaMMc95XwKsJkOK3HeTyH8vsOGVSzDmBvd1AsDqk5UalDmlRU1qq7MVdd7eim3i0fwEGSMFq</recordid><startdate>20141121</startdate><enddate>20141121</enddate><creator>Marjoram, Robin J</creator><creator>Li, Zhengzhi</creator><creator>He, Li</creator><creator>Tollefsen, Douglas M</creator><creator>Kunicki, Thomas J</creator><creator>Dickeson, S Kent</creator><creator>Santoro, Samuel A</creator><creator>Zutter, Mary M</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>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>5PM</scope><scope>DOA</scope></search><sort><creationdate>20141121</creationdate><title>α2β1 integrin, GPVI receptor, and common FcRγ chain on mouse platelets mediate distinct responses to collagen in models of thrombosis</title><author>Marjoram, Robin J ; Li, Zhengzhi ; He, Li ; Tollefsen, Douglas M ; Kunicki, Thomas J ; Dickeson, S Kent ; Santoro, Samuel A ; Zutter, Mary M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4415-7ef6ae9ee90cfa97c010cfa4942a79e0ec9724ffc189894715a6f26180adf1e43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Activation</topic><topic>Animal models</topic><topic>Animals</topic><topic>Biology and Life Sciences</topic><topic>Blood clots</topic><topic>Blood platelets</topic><topic>Blood Platelets - metabolism</topic><topic>Carotid artery</topic><topic>Cerebral blood flow</topic><topic>Chains</topic><topic>Collagen</topic><topic>Collagen (type I)</topic><topic>Collagen - adverse effects</topic><topic>Collagen - pharmacology</topic><topic>Disease Models, Animal</topic><topic>Genetic modification</topic><topic>Glycoprotein VI</topic><topic>Glycoproteins</topic><topic>Hemostasis</topic><topic>Hemostatics</topic><topic>Immunoglobulins</topic><topic>Immunology</topic><topic>Integrin alpha2beta1 - genetics</topic><topic>Integrin alpha2beta1 - metabolism</topic><topic>Ischemia</topic><topic>Medicine</topic><topic>Medicine and Health Sciences</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Mutation</topic><topic>Occlusion</topic><topic>Pathology</topic><topic>Phosphorylation</topic><topic>Phosphotyrosine</topic><topic>Platelet Activation - drug effects</topic><topic>Platelet Activation - genetics</topic><topic>Platelet Membrane Glycoproteins - genetics</topic><topic>Platelet Membrane Glycoproteins - metabolism</topic><topic>Platelets</topic><topic>Proteins</topic><topic>Rats</topic><topic>Receptor mechanisms</topic><topic>Receptors</topic><topic>Receptors, IgG - genetics</topic><topic>Receptors, IgG - metabolism</topic><topic>Research and Analysis Methods</topic><topic>Signaling</topic><topic>Thromboembolism</topic><topic>Thrombosis</topic><topic>Thrombosis - chemically induced</topic><topic>Thrombosis - genetics</topic><topic>Thrombosis - metabolism</topic><topic>Tyrosine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Marjoram, Robin J</creatorcontrib><creatorcontrib>Li, Zhengzhi</creatorcontrib><creatorcontrib>He, Li</creatorcontrib><creatorcontrib>Tollefsen, Douglas M</creatorcontrib><creatorcontrib>Kunicki, Thomas J</creatorcontrib><creatorcontrib>Dickeson, S Kent</creatorcontrib><creatorcontrib>Santoro, Samuel A</creatorcontrib><creatorcontrib>Zutter, Mary 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>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</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>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Understanding platelet-collagen receptor function has been enhanced through use of genetically modified mouse models. Previous studies of GPVI/FcRγ-mediated collagen-induced platelet activation were perfomed with mice in which the FcRγ subunit was genetically deleted (FcRγ-/-) or the complex was depleted. The development of α2β1-/- and GPVI-/- mice permits side-by-side comparison to address contributions of these collagen receptors in vivo and in vitro.
To understand the different roles played by the α2β1 integrin, the GPVI receptor or FcRγ subunit in collagen-stimulated hemostasis and thrombosis, we compared α2β1-/-, FcRγ-/-, and GPVI-/- mice in models of endothelial injury and intravascular thrombosis in vivo and their platelets in collagen-stimulated activation in vitro. We demonstrate that both the α2β1 integrin and the GPVI receptor, but not the FcRγ subunit influence carotid artery occlusion in vivo. In contrast, the GPVI receptor and the FcRγ chain, but not the α2β1 integrin, play similar roles in intravascular thrombosis in response to soluble Type I collagen. FcRγ-/- platelets showed less attenuation of tyrosine phosphorylation of several proteins including RhoGDI when compared to GPVI-/- and wild type platelets. The difference between FcRγ-/- and GPVI-/- platelet phosphotyrosine levels correlated with the in vivo thrombosis findings.
Our data demonstrate that genetic deletion of GPVI receptor, FcRγ chain, or the α2β1 integrin changes the thrombotic potentials of these platelets to collagen dependent on the stimulus mechanism. The data suggest that the FcRγ chain may provide a dominant negative effect through modulating signaling pathways in platelets involving several tyrosine phosphorylated proteins such as RhoGDI. In addition, these findings suggest a more complex signaling network downstream of the platelet collagen receptors than previously appreciated.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25415203</pmid><doi>10.1371/journal.pone.0114035</doi><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1626822586 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Activation Animal models Animals Biology and Life Sciences Blood clots Blood platelets Blood Platelets - metabolism Carotid artery Cerebral blood flow Chains Collagen Collagen (type I) Collagen - adverse effects Collagen - pharmacology Disease Models, Animal Genetic modification Glycoprotein VI Glycoproteins Hemostasis Hemostatics Immunoglobulins Immunology Integrin alpha2beta1 - genetics Integrin alpha2beta1 - metabolism Ischemia Medicine Medicine and Health Sciences Mice Mice, Knockout Mutation Occlusion Pathology Phosphorylation Phosphotyrosine Platelet Activation - drug effects Platelet Activation - genetics Platelet Membrane Glycoproteins - genetics Platelet Membrane Glycoproteins - metabolism Platelets Proteins Rats Receptor mechanisms Receptors Receptors, IgG - genetics Receptors, IgG - metabolism Research and Analysis Methods Signaling Thromboembolism Thrombosis Thrombosis - chemically induced Thrombosis - genetics Thrombosis - metabolism Tyrosine |
| title | α2β1 integrin, GPVI receptor, and common FcRγ chain on mouse platelets mediate distinct responses to collagen in models of thrombosis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-19T01%3A55%3A17IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=%CE%B12%CE%B21%20integrin,%20GPVI%20receptor,%20and%20common%20FcR%CE%B3%20chain%20on%20mouse%20platelets%20mediate%20distinct%20responses%20to%20collagen%20in%20models%20of%20thrombosis&rft.jtitle=PloS%20one&rft.au=Marjoram,%20Robin%20J&rft.date=2014-11-21&rft.volume=9&rft.issue=11&rft.spage=e114035&rft.pages=e114035-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0114035&rft_dat=%3Cproquest_plos_%3E3503716621%3C/proquest_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1626822586&rft_id=info:pmid/25415203&rft_doaj_id=oai_doaj_org_article_a0186060a2c64848bb49810c27afac21&rfr_iscdi=true |