{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T18:04:49Z","timestamp":1792087489298,"version":"4.4.0"},"reference-count":55,"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":[[2025,10]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND:<\/jats:title>\n            <jats:p>Neutrophil infiltration exacerbates brain injury after subarachnoid hemorrhage (SAH). Integrin \u03b19, expressed on neutrophils, facilitates their adhesion and transendothelial migration, leading to aggravated inflammatory responses and neuronal apoptosis. Insufficient clearance of apoptotic neurons by microglia and infiltrating blood-derived macrophages (defective efferocytosis) contributes to persistent inflammation and poor SAH recovery. This study investigated the role of neutrophil integrin \u03b19 in neuronal apoptosis, microglia\/macrophage efferocytosis, and SAH outcomes.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS:<\/jats:title>\n            <jats:p>\n              Neutrophil-specific\n              <jats:italic toggle=\"yes\">\u03b19<\/jats:italic>\n              <jats:sup>\n                <jats:italic toggle=\"yes\">\u2013\/\u2013<\/jats:italic>\n              <\/jats:sup>\n              (\n              <jats:italic toggle=\"yes\">\u03b19<\/jats:italic>\n              <jats:sup>\n                <jats:italic toggle=\"yes\">fl\/fl<\/jats:italic>\n              <\/jats:sup>\n              <jats:italic toggle=\"yes\">Mrp8Cre<\/jats:italic>\n              <jats:sup>\n                <jats:italic toggle=\"yes\">\u2013\/+<\/jats:italic>\n              <\/jats:sup>\n              ) and littermate control (\n              <jats:italic toggle=\"yes\">\u03b19<\/jats:italic>\n              <jats:sup>\n                <jats:italic toggle=\"yes\">fl\/fl<\/jats:italic>\n              <\/jats:sup>\n              <jats:italic toggle=\"yes\">Mrp8Cre<\/jats:italic>\n              <jats:sup>\n                <jats:italic toggle=\"yes\">\u2013\/\u2013<\/jats:italic>\n              <\/jats:sup>\n              ) mice were subjected to the endovascular perforation model to induce SAH. Sensorimotor and cognitive function were assessed for up to 4 weeks post-SAH using neurological severity score, corner and cylinder tests, Y-maze, and novel object recognition. In vitro and in vivo functional assays were conducted to assess the effect of integrin \u03b19\u2013dependent neutrophil transendothelial migration on efferocytosis of apoptotic neurons. Neutrophil infiltration, cerebral inflammation, neuronal apoptosis, and MMP (matrix metalloproteinase)-9 were quantified 24 hours post-SAH.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>RESULTS:<\/jats:title>\n            <jats:p>\n              Mice subjected to SAH exhibited increased integrin \u03b19 levels on infiltrated neutrophils compared with sham surgery controls. Neutrophil-specific\n              <jats:italic toggle=\"yes\">\u03b19<\/jats:italic>\n              <jats:sup>\n                <jats:italic toggle=\"yes\">\u2013\/\u2013<\/jats:italic>\n              <\/jats:sup>\n              mice demonstrated improved long-term sensorimotor and cognitive recovery, reduced neutrophil infiltration, and decreased MMP-9 expression and neuronal apoptosis. Importantly, neutrophil-specific\n              <jats:italic toggle=\"yes\">\u03b19<\/jats:italic>\n              <jats:sup>\n                <jats:italic toggle=\"yes\">\u2013\/\u2013<\/jats:italic>\n              <\/jats:sup>\n              mice exhibited reduced brain neutrophil elastase levels and enhanced efferocytosis. Mechanistic studies have revealed that the reduced transendothelial migration of\n              <jats:italic toggle=\"yes\">\u03b19<\/jats:italic>\n              <jats:sup>\n                <jats:italic toggle=\"yes\">\u2013\/\u2013<\/jats:italic>\n              <\/jats:sup>\n              neutrophils directly contributed to the enhanced microglia\/macrophage efferocytosis of apoptotic neurons. Pharmacological targeting of integrin \u03b19 with macitentan significantly improved SAH outcomes by reducing neutrophil infiltration and enhancing efferocytosis. Comparable SAH outcomes in both macitentan-treated controls and neutrophil-specific\n              <jats:italic toggle=\"yes\">\u03b19<\/jats:italic>\n              <jats:sup>\n                <jats:italic toggle=\"yes\">\u2013\/\u2013<\/jats:italic>\n              <\/jats:sup>\n              mice suggested that the therapeutic effects of macitentan were mediated by inhibition of neutrophil integrin \u03b19.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS:<\/jats:title>\n            <jats:p>Our study revealed a novel role for neutrophil integrin \u03b19 in sensorimotor function and cognitive recovery after SAH, suggesting it as a potential therapeutic target for SAH.<\/jats:p>\n          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