{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,30]],"date-time":"2026-06-30T03:32:38Z","timestamp":1782790358944,"version":"3.54.5"},"reference-count":36,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"10","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2024,10]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND:<\/jats:title>\n            <jats:p>Platelets prevent bleeding in a variety of inflammatory settings, the adhesion receptors and activation pathways involved being highly context-dependent and functionally redundant. In some situations, platelets recruited to inflammatory sites act independently of aggregation. The mechanisms underlying stable platelet adhesion in inflamed microvessels remain incompletely understood, in particular, whether and if so, how \u03b21 and \u03b23 integrins are involved.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS:<\/jats:title>\n            <jats:p>The impact of isolated or combined platelet deficiency in \u03b21 and \u03b23 integrins on inflammation-associated hemostasis was investigated in 3 models of acute inflammation: immune complex-based cutaneous reverse passive Arthus reaction, intranasal lipopolysaccharide-induced lung inflammation, and cerebral ischemia-reperfusion following transient (2-hour) occlusion of the middle cerebral artery.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>RESULTS:<\/jats:title>\n            <jats:p>\n              Mice with platelet-directed inactivation of\n              <jats:italic toggle=\"yes\">Itgb1<\/jats:italic>\n              (PF4Cre-\u03b21\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              ) displayed no bleeding in any of the inflammation models, while mice defective in platelet\n              <jats:italic toggle=\"yes\">Itgb3<\/jats:italic>\n              (PF4Cre-\u03b23\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              ) exhibited bleeding in all 3 models. Remarkably, the bleeding phenotype of PF4Cre-\u03b23\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice was exacerbated in the reverse passive Arthus model by the concomitant deletion of \u03b21 integrins, PF4Cre-\u03b21\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              \/\u03b23\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              animals presenting increased bleeding. Intravital microscopy in reverse passive Arthus experiments highlighted a major defect in the adhesion of PF4Cre-\u03b21\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              \/\u03b23\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              platelets to inflamed microvessels. Unlike PF4Cre-\u03b21\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              and PF4Cre-\u03b23\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice, PF4Cre-\u03b21\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              \/\u03b23\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              animals developed early hemorrhagic transformation 6 hours after transient middle cerebral artery occlusion. PF4Cre-\u03b21\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              \/\u03b23\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice displayed no more bleeding in lipopolysaccharide-induced lung inflammation than PF4Cre-\u03b23\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              animals.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS:<\/jats:title>\n            <jats:p>Altogether, these results show that the requirement for and degree of functional redundancy between platelet \u03b21 and \u03b23 integrins in inflammation-associated hemostasis vary with the inflammatory situation.<\/jats:p>\n          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Strasbourg), Universit\u00e9 de Strasbourg, France (E.J.-B., N.R., L.M., C.M., S.M., F.L., B.H., P.H.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicolas","family":"Receveur","sequence":"additional","affiliation":[{"name":"Institut national de la sant\u00e9 et de la recherche m\u00e9dicale (INSERM), EFS (Etablissement fran\u00e7ais du sang) Grand Est, BPPS (Biologie et pharmacologie des plaquettes sanguines: h\u00e9mostase, thrombose, transfusion) UMR (Unit\u00e9 mixte de recherche)-S1255, FMTS (F\u00e9d\u00e9ration de m\u00e9decine translationnelle de Strasbourg), Universit\u00e9 de Strasbourg, France (E.J.-B., N.R., L.M., C.M., S.M., F.L., B.H., P.H.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5866-2547","authenticated-orcid":true,"given":"Luc","family":"Mercier","sequence":"additional","affiliation":[{"name":"Institut national de la sant\u00e9 et de la recherche m\u00e9dicale (INSERM), EFS (Etablissement fran\u00e7ais du sang) Grand Est, BPPS (Biologie et pharmacologie des plaquettes sanguines: h\u00e9mostase, thrombose, transfusion) UMR (Unit\u00e9 mixte de recherche)-S1255, FMTS (F\u00e9d\u00e9ration de m\u00e9decine translationnelle de Strasbourg), Universit\u00e9 de Strasbourg, France (E.J.-B., N.R., L.M., C.M., S.M., F.L., B.H., P.H.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0817-7818","authenticated-orcid":true,"given":"Clarisse","family":"Mouriaux","sequence":"additional","affiliation":[{"name":"Institut national de la sant\u00e9 et de la recherche m\u00e9dicale (INSERM), EFS (Etablissement fran\u00e7ais du sang) Grand Est, BPPS (Biologie et pharmacologie des plaquettes sanguines: h\u00e9mostase, thrombose, transfusion) UMR (Unit\u00e9 mixte de recherche)-S1255, FMTS (F\u00e9d\u00e9ration de m\u00e9decine translationnelle de Strasbourg), Universit\u00e9 de Strasbourg, France (E.J.-B., N.R., L.M., C.M., 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