{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T23:00:53Z","timestamp":1793314853066,"version":"4.5.0"},"reference-count":66,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","license":[{"start":{"date-parts":[[2022,1,1]],"date-time":"2022-01-01T00:00:00Z","timestamp":1640995200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2022,1]]},"abstract":"<jats:sec>\n            <jats:title>Objective:<\/jats:title>\n            <jats:p>Platelets are central to acute myocardial infarction (MI). How the platelet proteome is altered during MI is unknown. We sought to describe changes in the platelet proteome during MI and identify corresponding functional consequences.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results:<\/jats:title>\n            <jats:p>\n              Platelets from patients experiencing ST-segment\u2013elevation MI (STEMI) before and 3 days after treatment (n=30) and matched patients with severe stable coronary artery disease before and 3 days after coronary artery bypass grafting (n=25) underwent quantitative proteomic analysis. Elevations in the proteins S100A8 and S100A9 were detected at the time of STEMI compared with stable coronary artery disease (S100A8: FC, 2.00; false discovery rate, 0.05; S100A9: FC, 2.28; false discovery rate, 0.005). During STEMI, only S100A8 mRNA and protein levels were correlated in platelets (\n              <jats:italic>R<\/jats:italic>\n              =0.46,\n              <jats:italic>P<\/jats:italic>\n              =0.012). To determine whether de novo protein synthesis occurs, activated platelets were incubated with 13C-labeled amino acids for 24 hours and analyzed by mass spectrometry. No incorporation was confidently detected. Platelet S100A8 and S100A9 was strongly correlated with neutrophil abundance at the time of STEMI. When isolated platelets and neutrophils were coincubated under quiescent and activated conditions, release of S100A8 from neutrophils resulted in uptake of S100A8 by platelets. Neutrophils released S100A8\/A9 as free heterodimer, rather than in vesicles or extracellular traps. In the community-based Bruneck study (n=338), plasma S100A8\/A9 was inversely associated with platelet reactivity\u2014an effect abrogated by aspirin.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions:<\/jats:title>\n            <jats:p>Leukocyte-to-platelet protein transfer may occur in a thromboinflammatory environment such as STEMI. Plasma S100A8\/A9 was negatively associated with platelet reactivity. These findings highlight neutrophils as potential modifiers for thrombotic therapies in coronary artery disease.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.121.317113","type":"journal-article","created":{"date-parts":[[2021,11,23]],"date-time":"2021-11-23T10:00:50Z","timestamp":1637661650000},"page":"49-62","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":61,"title":["Neutrophil-Derived Protein S100A8\/A9 Alters the Platelet Proteome in Acute Myocardial Infarction and Is Associated With Changes in Platelet Reactivity"],"prefix":"10.1161","volume":"42","author":[{"given":"Abhishek","family":"Joshi","sequence":"first","affiliation":[{"name":"King\u2019s College London British Heart Foundation Centre, School of Cardiovascular Medicine and Sciences, United Kingdom (A.J., L.E.S., S.A.B., R.L., F.B., C.G., T.B., K.T., M.M.)."},{"name":"Department of Cardiology, Barts Heart Centre, St. Bartholomew\u2019s Hospital, London, United Kingdom (A.J., A.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7565-1455","authenticated-orcid":true,"given":"Lukas E.","family":"Schmidt","sequence":"additional","affiliation":[{"name":"King\u2019s College London British Heart Foundation Centre, School of Cardiovascular Medicine and Sciences, United Kingdom (A.J., L.E.S., S.A.B., R.L., F.B., C.G., T.B., K.T., M.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sean A.","family":"Burnap","sequence":"additional","affiliation":[{"name":"King\u2019s College London British Heart Foundation Centre, School of Cardiovascular Medicine and Sciences, United Kingdom (A.J., L.E.S., S.A.B., R.L., F.B., C.G., T.B., K.T., M.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruifang","family":"Lu","sequence":"additional","affiliation":[{"name":"King\u2019s College London British Heart Foundation Centre, School of Cardiovascular Medicine and 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