{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,25]],"date-time":"2025-10-25T12:12:30Z","timestamp":1761394350618},"reference-count":21,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2013,9]]},"abstract":"<jats:sec>\n            <jats:title>Objective\u2014<\/jats:title>\n            <jats:p>To investigate the role of acyl-CoA:cholesterol acyltransferase 1 (ACAT1) in hematopoiesis.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results\u2014<\/jats:title>\n            <jats:p>\n              ACAT1 converts cellular cholesterol to cholesteryl esters for storage in multiple cell types and is a potential drug target for human diseases. In mouse models for atherosclerosis, global\n              <jats:italic>Acat1<\/jats:italic>\n              knockout causes increased lesion size; bone marrow transplantation experiments suggest that the increased lesion size might be caused by ACAT1 deficiency in macrophages. However, bone marrow contains hematopoietic stem cells that give rise to cells in myeloid and lymphoid lineages; these cell types affect atherosclerosis at various stages. Here, we test the hypothesis that global\n              <jats:italic>Acat1<\/jats:italic>\n              <jats:sup>\n                <jats:italic>\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              may affect hematopoiesis, rather than affecting macrophage function only, and show that\n              <jats:italic>Acat1<\/jats:italic>\n              <jats:sup>\n                <jats:italic>\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              mice contain significantly higher numbers of myeloid cells and other cells than wild-type mice. Detailed analysis of bone marrow cells demonstrated that\n              <jats:italic>Acat1<\/jats:italic>\n              <jats:sup>\n                <jats:italic>\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              causes a higher proportion of the stem cell\u2013enriched Lin\n              <jats:sup>\u2212<\/jats:sup>\n              Sca-1\n              <jats:sup>+<\/jats:sup>\n              c-Kit\n              <jats:sup>+<\/jats:sup>\n              population to proliferate, resulting in higher numbers of myeloid progenitor cells. In addition, we show that\n              <jats:italic>Acat1<\/jats:italic>\n              <jats:sup>\n                <jats:italic>\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              causes higher monocytosis in\n              <jats:italic>Apoe<\/jats:italic>\n              <jats:sup>\n                <jats:italic>\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              mouse during atherosclerosis development.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions\u2014<\/jats:title>\n            <jats:p>\n              ACAT1 plays important roles in hematopoiesis in normal mouse and in\n              <jats:italic>Apoe<\/jats:italic>\n              <jats:sup>\n                <jats:italic>\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              mouse during atherosclerosis development.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.112.301080","type":"journal-article","created":{"date-parts":[[2013,7,12]],"date-time":"2013-07-12T05:39:07Z","timestamp":1373607547000},"page":"2081-2087","update-policy":"http:\/\/dx.doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":17,"title":["<i>Acat1<\/i>\n            Gene Ablation in Mice Increases Hematopoietic Progenitor Cell Proliferation in Bone Marrow and Causes Leukocytosis"],"prefix":"10.1161","volume":"33","author":[{"given":"Li-Hao","family":"Huang","sequence":"first","affiliation":[{"name":"From the Department of Biochemistry (L.-H.H., C.C.Y.C., T.-Y.C.), Department of Pharmacology (J.G., R.C.), Department of Genetics (E.A., P.A.E.), and Department of Immunology (B.L.B.), Geisel School of Medicine at Dartmouth, Hanover, NH."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jingang","family":"Gui","sequence":"additional","affiliation":[{"name":"From the Department of Biochemistry (L.-H.H., C.C.Y.C., T.-Y.C.), Department of Pharmacology (J.G., R.C.), Department of Genetics (E.A., P.A.E.), and Department of Immunology (B.L.B.), Geisel School of Medicine at Dartmouth, Hanover, NH."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Erika","family":"Artinger","sequence":"additional","affiliation":[{"name":"From the Department of Biochemistry (L.-H.H., C.C.Y.C., T.-Y.C.), Department of Pharmacology (J.G., R.C.), Department of Genetics (E.A., P.A.E.), and Department of Immunology (B.L.B.), Geisel School of Medicine at Dartmouth, Hanover, NH."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ruth","family":"Craig","sequence":"additional","affiliation":[{"name":"From the Department of Biochemistry (L.-H.H., C.C.Y.C., T.-Y.C.), Department of Pharmacology (J.G., R.C.), Department of Genetics (E.A., P.A.E.), and Department of Immunology (B.L.B.), Geisel School of Medicine at Dartmouth, Hanover, NH."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brent L.","family":"Berwin","sequence":"additional","affiliation":[{"name":"From the Department of Biochemistry (L.-H.H., C.C.Y.C., T.-Y.C.), Department of Pharmacology (J.G., R.C.), Department of Genetics (E.A., P.A.E.), and Department of Immunology (B.L.B.), Geisel School of Medicine at Dartmouth, Hanover, NH."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Patricia A.","family":"Ernst","sequence":"additional","affiliation":[{"name":"From the Department of Biochemistry (L.-H.H., C.C.Y.C., T.-Y.C.), Department of Pharmacology (J.G., R.C.), Department of Genetics (E.A., P.A.E.), and Department of Immunology (B.L.B.), Geisel School of Medicine at Dartmouth, Hanover, NH."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Catherine C.Y.","family":"Chang","sequence":"additional","affiliation":[{"name":"From the Department of Biochemistry (L.-H.H., C.C.Y.C., T.-Y.C.), Department of Pharmacology (J.G., R.C.), Department of Genetics (E.A., P.A.E.), and Department of Immunology (B.L.B.), Geisel School of Medicine at Dartmouth, Hanover, NH."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ta-Yuan","family":"Chang","sequence":"additional","affiliation":[{"name":"From the Department of Biochemistry (L.-H.H., C.C.Y.C., T.-Y.C.), Department of Pharmacology (J.G., R.C.), Department of Genetics (E.A., P.A.E.), and Department of Immunology (B.L.B.), Geisel School of Medicine at Dartmouth, Hanover, NH."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_4_2_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.90926.2008"},{"key":"e_1_3_4_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1388-1981(00)00144-X"},{"key":"e_1_3_4_4_2","doi-asserted-by":"publisher","DOI":"10.1097\/00041433-200104000-00005"},{"key":"e_1_3_4_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64723-2"},{"key":"e_1_3_4_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-2275(20)32360-9"},{"key":"e_1_3_4_7_2","doi-asserted-by":"publisher","DOI":"10.1097\/01.LAB.0000095687.17383.39"},{"key":"e_1_3_4_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.atherosclerosis.2010.08.048"},{"key":"e_1_3_4_9_2","doi-asserted-by":"publisher","DOI":"10.1161\/atvbaha.112.252056"},{"key":"e_1_3_4_10_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI9021"},{"key":"e_1_3_4_11_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI10310"},{"key":"e_1_3_4_12_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1189731"},{"key":"e_1_3_4_13_2","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2010.091063"},{"key":"e_1_3_4_14_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri1780"},{"key":"e_1_3_4_15_2","first-page":"757","article-title":"A 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A preliminary report: preparations containing Interleukin-3 (IL-3) promote proliferation of multipotential stem cells (CFUs) in the mouse. 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