{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,3]],"date-time":"2026-07-03T04:16:01Z","timestamp":1783052161662,"version":"3.54.6"},"reference-count":63,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"24","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2025,6,17]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND:<\/jats:title>\n            <jats:p>Immune cells are closely associated with all processes of cardiac repair after myocardial infarction (MI), including the initiation, development, and resolution of inflammation. Spleen extramedullary hematopoiesis (EMH) serves as a crucial source of emergency mature blood cells that are generated through the self-renewal and differentiation of hematopoietic stem\/progenitor cells (HSPCs). However, how EMH responds to MI and the role of EMH in cardiac repair after MI remains unclear.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS:<\/jats:title>\n            <jats:p>\n              To assess the role of spleen EMH in MI, a\n              <jats:italic toggle=\"yes\">Tcf21<\/jats:italic>\n              <jats:sup>\n                <jats:italic toggle=\"yes\">CreER<\/jats:italic>\n              <\/jats:sup>\n              <jats:italic toggle=\"yes\">Scf<\/jats:italic>\n              <jats:sup>\n                <jats:italic toggle=\"yes\">flox\/flox<\/jats:italic>\n              <\/jats:sup>\n              MI mouse model with inhibited EMH was constructed. GFP\n              <jats:sup>+<\/jats:sup>\n              (green fluorescent protein) hematopoietic stem cells were sorted from eGFP (enhanced GFP) mouse spleen by flow cytometry and injected into\n              <jats:italic toggle=\"yes\">Tcf21<\/jats:italic>\n              <jats:sup>\n                <jats:italic toggle=\"yes\">CreER<\/jats:italic>\n              <\/jats:sup>\n              <jats:italic toggle=\"yes\">Scf<\/jats:italic>\n              <jats:sup>\n                <jats:italic toggle=\"yes\">flox\/flox<\/jats:italic>\n              <\/jats:sup>\n              mice to test the sources of local inflammatory cells during MI. Using highly specific liquid chromatography\u2013tandem mass spectrometry and single-cell RNA sequencing, we analyzed the lipidomic profile of arachidonic acid metabolites and the transcriptomes of HSPCs in the spleen after MI.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>RESULTS:<\/jats:title>\n            <jats:p>\n              We found that MI enhanced EMH, as reflected by the increase in spleen weight and volume and the number of HSPCs in the spleen. The lack of EMH in\n              <jats:italic toggle=\"yes\">Scf<\/jats:italic>\n              -deficient mice exacerbated tissue injury after MI. Analysis of the transcriptome of spleen HSPCs after MI revealed that the type 1 interferon pathway was substantially inhibited in hematopoietic stem cell \/multipotent progenitor subclusters, and the absence of type 1 interferon signaling enhanced the MI-induced spleen EMH. Lipidomics analysis revealed that prostaglandin I2 (PGI2) was markedly reduced in the spleen. PGI2 suppressed MI-induced EMH through a PGI2 receptor (IP)\u2013cyclic adenosine monophosphate\u2013\n              <jats:sup>453<\/jats:sup>\n              p-SP1 cascade in spleen HSPCs. Hematopoietic cell\u2013specific IP-deficient mice exhibited enhanced EMH and improved cardiac recovery after MI.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS:<\/jats:title>\n            <jats:p>Together, our findings revealed that a PGI2\u2013IFN axis was involved in spleen EMH after MI, providing new mechanistic insights into spleen EMH after MI and offering a new therapeutic target for treating ischemic cardiac injury.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circulationaha.124.069420","type":"journal-article","created":{"date-parts":[[2025,4,28]],"date-time":"2025-04-28T09:00:47Z","timestamp":1745830847000},"page":"1730-1747","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":13,"title":["Suppression of the Prostaglandin I2\u2013Type 1 Interferon Axis Induces Extramedullary Hematopoiesis to Promote Cardiac Repair After Myocardial Infarction"],"prefix":"10.1161","volume":"151","author":[{"given":"Huizhen","family":"Lv","sequence":"first","affiliation":[{"name":"State Key Laboratory of Experimental Hematology, Tianjin Institute of Cardiology, Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Second Hospital of Tianjin Medical University, and Department of Physiology and Pathophysiology (H.L., Z.L., M.Q., K.L., X.S., D.A.), Tianjin Medical University, China."},{"name":"Department of Cardiology, Peking University First Hospital, Beijing, China (H.L., D.A.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chenchen","family":"Wang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology &amp; 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