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Homophilic Interaction Between Transmembrane-JAM-A and Soluble JAM-A Regulates Thrombo-Inflammation: Implications for Coronary Artery Disease
Genetic predisposition through single-nucleotide variation (SNV) influences circulatory soluble junctional adhesion molecule-A (sJAM-A) levels in coronary artery disease (CAD) patients. Homozygous carriers of the minor alleles ( SNVs rs2774276, rs790056) show enhanced levels of thrombo-inflammatory...
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| Published in: | JACC. Basic to translational science 2022-05, Vol.7 (5), p.445-461 |
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| Main Authors: | , , , , , , , , , , , , , , , , , , , , , , |
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| container_title | JACC. Basic to translational science |
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| creator | Rath, Dominik Rapp, Vera Schwartz, Jessica Winter, Stefan Emschermann, Frederic Arnold, Daniel Rheinlaender, Johannes Büttcher, Manuela Strebl, Michael Braun, Michael B Altgelt, Konstanze Uribe, Álvaro Petersen Schories, Christoph Canjuga, Denis Schaeffeler, Elke Borst, Oliver Schäffer, Tilman E Langer, Harald Stehle, Thilo Schwab, Matthias Geisler, Tobias Gawaz, Meinrad Chatterjee, Madhumita |
| description | Genetic predisposition through
single-nucleotide variation (SNV) influences circulatory soluble junctional adhesion molecule-A (sJAM-A) levels in coronary artery disease (CAD) patients. Homozygous carriers of the minor alleles (
SNVs rs2774276, rs790056) show enhanced levels of thrombo-inflammatory sJAM-A. Both
SNVs and sJAM-A are associated with worse prognosis for recurrent myocardial infarction in CAD patients. Platelet surface-associated JAM-A correlate with platelet activation markers in CAD patients. Activated platelets shed transmembrane-JAM-A, generating proinflammatory sJAM-A and JAM-A-bearing microparticles. Platelet transmembrane-JAM-A and sJAM-A as homophilic interaction partners exaggerate thrombotic and thrombo-inflammatory platelet monocyte interactions. Therapeutic strategies interfering with this homophilic interface may regulate thrombotic and thrombo-inflammatory platelet response in cardiovascular pathologies where circulatory sJAM-A levels are elevated. |
| doi_str_mv | 10.1016/j.jacbts.2022.03.003 |
| format | article |
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SNVs rs2774276, rs790056) show enhanced levels of thrombo-inflammatory sJAM-A. Both
SNVs and sJAM-A are associated with worse prognosis for recurrent myocardial infarction in CAD patients. Platelet surface-associated JAM-A correlate with platelet activation markers in CAD patients. Activated platelets shed transmembrane-JAM-A, generating proinflammatory sJAM-A and JAM-A-bearing microparticles. Platelet transmembrane-JAM-A and sJAM-A as homophilic interaction partners exaggerate thrombotic and thrombo-inflammatory platelet monocyte interactions. Therapeutic strategies interfering with this homophilic interface may regulate thrombotic and thrombo-inflammatory platelet response in cardiovascular pathologies where circulatory sJAM-A levels are elevated.</description><identifier>EISSN: 2452-302X</identifier><identifier>DOI: 10.1016/j.jacbts.2022.03.003</identifier><identifier>PMID: 35663628</identifier><language>eng</language><publisher>United States: Elsevier</publisher><subject>Leading Edge Translational Research</subject><ispartof>JACC. Basic to translational science, 2022-05, Vol.7 (5), p.445-461</ispartof><rights>2022 The Authors.</rights><rights>2022 The Authors 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9156439/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9156439/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35663628$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rath, Dominik</creatorcontrib><creatorcontrib>Rapp, Vera</creatorcontrib><creatorcontrib>Schwartz, Jessica</creatorcontrib><creatorcontrib>Winter, Stefan</creatorcontrib><creatorcontrib>Emschermann, Frederic</creatorcontrib><creatorcontrib>Arnold, Daniel</creatorcontrib><creatorcontrib>Rheinlaender, Johannes</creatorcontrib><creatorcontrib>Büttcher, Manuela</creatorcontrib><creatorcontrib>Strebl, Michael</creatorcontrib><creatorcontrib>Braun, Michael B</creatorcontrib><creatorcontrib>Altgelt, Konstanze</creatorcontrib><creatorcontrib>Uribe, Álvaro Petersen</creatorcontrib><creatorcontrib>Schories, Christoph</creatorcontrib><creatorcontrib>Canjuga, Denis</creatorcontrib><creatorcontrib>Schaeffeler, Elke</creatorcontrib><creatorcontrib>Borst, Oliver</creatorcontrib><creatorcontrib>Schäffer, Tilman E</creatorcontrib><creatorcontrib>Langer, Harald</creatorcontrib><creatorcontrib>Stehle, Thilo</creatorcontrib><creatorcontrib>Schwab, Matthias</creatorcontrib><creatorcontrib>Geisler, Tobias</creatorcontrib><creatorcontrib>Gawaz, Meinrad</creatorcontrib><creatorcontrib>Chatterjee, Madhumita</creatorcontrib><title>Homophilic Interaction Between Transmembrane-JAM-A and Soluble JAM-A Regulates Thrombo-Inflammation: Implications for Coronary Artery Disease</title><title>JACC. Basic to translational science</title><addtitle>JACC Basic Transl Sci</addtitle><description>Genetic predisposition through
single-nucleotide variation (SNV) influences circulatory soluble junctional adhesion molecule-A (sJAM-A) levels in coronary artery disease (CAD) patients. Homozygous carriers of the minor alleles (
SNVs rs2774276, rs790056) show enhanced levels of thrombo-inflammatory sJAM-A. Both
SNVs and sJAM-A are associated with worse prognosis for recurrent myocardial infarction in CAD patients. Platelet surface-associated JAM-A correlate with platelet activation markers in CAD patients. Activated platelets shed transmembrane-JAM-A, generating proinflammatory sJAM-A and JAM-A-bearing microparticles. Platelet transmembrane-JAM-A and sJAM-A as homophilic interaction partners exaggerate thrombotic and thrombo-inflammatory platelet monocyte interactions. Therapeutic strategies interfering with this homophilic interface may regulate thrombotic and thrombo-inflammatory platelet response in cardiovascular pathologies where circulatory sJAM-A levels are elevated.</description><subject>Leading Edge Translational Research</subject><issn>2452-302X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><recordid>eNpVkc9O3DAQxi0kVBDwBgj52EvSsZ04CYdKy7bAVlSVYA_cIjs7YbPyn2AnRTxE37lugaqcRjPz6ft9miHklEHOgMlPu3ynOj3FnAPnOYgcQOyRQ16UPBPA7w_ISYw7gKQVVV2XH8iBKKUUkteH5Ne1t37cDmbo6MpNGFQ3Dd7RC5yeEB1dB-WiRatTxezb4nu2oMpt6J03szZIXya3-DAbNWGk623wVvts5XqjrFV_zM7pyo4J8LeJtPeBLn3wToVnugiJ-Uy_DBFVxGOy3ysT8eS1HpH15df18jq7-XG1Wi5uspHVbMo44w3ovq5kiVpqzbUURc-hYaKrQDQADULBeoZQ9pXWHW6UEKAQQeu-Ekfk84vtOGuLmw7dFJRpxzDYlKn1amjfb9ywbR_8z7ZhpSxEkww-vhoE_zhjnFo7xA6NSUfyc2y5rIoUghUsSc_-Z_2DvL1A_AaqLYyj</recordid><startdate>20220501</startdate><enddate>20220501</enddate><creator>Rath, Dominik</creator><creator>Rapp, Vera</creator><creator>Schwartz, Jessica</creator><creator>Winter, Stefan</creator><creator>Emschermann, Frederic</creator><creator>Arnold, Daniel</creator><creator>Rheinlaender, Johannes</creator><creator>Büttcher, Manuela</creator><creator>Strebl, Michael</creator><creator>Braun, Michael B</creator><creator>Altgelt, Konstanze</creator><creator>Uribe, Álvaro Petersen</creator><creator>Schories, Christoph</creator><creator>Canjuga, Denis</creator><creator>Schaeffeler, Elke</creator><creator>Borst, Oliver</creator><creator>Schäffer, Tilman E</creator><creator>Langer, Harald</creator><creator>Stehle, Thilo</creator><creator>Schwab, Matthias</creator><creator>Geisler, Tobias</creator><creator>Gawaz, Meinrad</creator><creator>Chatterjee, Madhumita</creator><general>Elsevier</general><scope>NPM</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20220501</creationdate><title>Homophilic Interaction Between Transmembrane-JAM-A and Soluble JAM-A Regulates Thrombo-Inflammation: Implications for Coronary Artery Disease</title><author>Rath, Dominik ; Rapp, Vera ; Schwartz, Jessica ; Winter, Stefan ; Emschermann, Frederic ; Arnold, Daniel ; Rheinlaender, Johannes ; Büttcher, Manuela ; Strebl, Michael ; Braun, Michael B ; Altgelt, Konstanze ; Uribe, Álvaro Petersen ; Schories, Christoph ; Canjuga, Denis ; Schaeffeler, Elke ; Borst, Oliver ; Schäffer, Tilman E ; Langer, Harald ; Stehle, Thilo ; Schwab, Matthias ; Geisler, Tobias ; Gawaz, Meinrad ; Chatterjee, Madhumita</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p181t-21290bf8765eb6bb2b634f20913c7039009e041f1e05f7bbceda330aee0bbf73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Leading Edge Translational Research</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rath, Dominik</creatorcontrib><creatorcontrib>Rapp, Vera</creatorcontrib><creatorcontrib>Schwartz, Jessica</creatorcontrib><creatorcontrib>Winter, Stefan</creatorcontrib><creatorcontrib>Emschermann, Frederic</creatorcontrib><creatorcontrib>Arnold, Daniel</creatorcontrib><creatorcontrib>Rheinlaender, Johannes</creatorcontrib><creatorcontrib>Büttcher, Manuela</creatorcontrib><creatorcontrib>Strebl, Michael</creatorcontrib><creatorcontrib>Braun, Michael B</creatorcontrib><creatorcontrib>Altgelt, Konstanze</creatorcontrib><creatorcontrib>Uribe, Álvaro Petersen</creatorcontrib><creatorcontrib>Schories, Christoph</creatorcontrib><creatorcontrib>Canjuga, Denis</creatorcontrib><creatorcontrib>Schaeffeler, Elke</creatorcontrib><creatorcontrib>Borst, Oliver</creatorcontrib><creatorcontrib>Schäffer, Tilman E</creatorcontrib><creatorcontrib>Langer, Harald</creatorcontrib><creatorcontrib>Stehle, Thilo</creatorcontrib><creatorcontrib>Schwab, Matthias</creatorcontrib><creatorcontrib>Geisler, Tobias</creatorcontrib><creatorcontrib>Gawaz, Meinrad</creatorcontrib><creatorcontrib>Chatterjee, Madhumita</creatorcontrib><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>JACC. 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single-nucleotide variation (SNV) influences circulatory soluble junctional adhesion molecule-A (sJAM-A) levels in coronary artery disease (CAD) patients. Homozygous carriers of the minor alleles (
SNVs rs2774276, rs790056) show enhanced levels of thrombo-inflammatory sJAM-A. Both
SNVs and sJAM-A are associated with worse prognosis for recurrent myocardial infarction in CAD patients. Platelet surface-associated JAM-A correlate with platelet activation markers in CAD patients. Activated platelets shed transmembrane-JAM-A, generating proinflammatory sJAM-A and JAM-A-bearing microparticles. Platelet transmembrane-JAM-A and sJAM-A as homophilic interaction partners exaggerate thrombotic and thrombo-inflammatory platelet monocyte interactions. Therapeutic strategies interfering with this homophilic interface may regulate thrombotic and thrombo-inflammatory platelet response in cardiovascular pathologies where circulatory sJAM-A levels are elevated.</abstract><cop>United States</cop><pub>Elsevier</pub><pmid>35663628</pmid><doi>10.1016/j.jacbts.2022.03.003</doi><tpages>17</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Leading Edge Translational Research |
| title | Homophilic Interaction Between Transmembrane-JAM-A and Soluble JAM-A Regulates Thrombo-Inflammation: Implications for Coronary Artery Disease |
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