{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T06:53:56Z","timestamp":1788850436169,"version":"build-2803163510"},"reference-count":102,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2016,10,26]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">Atherosclerosis is a chronic inflammatory disorder whose development is inversely correlated with high\u2010density lipoprotein concentration. Current therapies involve pharmaceuticals that significantly elevate plasma high\u2010density lipoprotein cholesterol concentrations. Our studies were conducted to investigate the effects of low\u2010dose lipid\u2010free apolipoprotein A\u2010I (apoA\u2010I) on chronic inflammation. The aims of these studies were to determine how subcutaneously injected lipid\u2010free apoA\u2010I reduces accumulation of lipid and immune cells within the aortic root of hypercholesterolemic mice without sustained elevations in plasma high\u2010density lipoprotein cholesterol concentrations.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              <jats:italic>Ldlr<\/jats:italic>\n              <jats:sup>\n                <jats:italic>\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              and\n              <jats:italic>Ldlr<\/jats:italic>\n              <jats:sup>\n                <jats:italic>\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              <jats:italic>apoA\u2010I<\/jats:italic>\n              <jats:sup>\n                <jats:italic>\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              mice were fed a Western diet for a total of 12\u00a0weeks. After 6\u00a0weeks, a subset of mice from each group received subcutaneous injections of 200\u00a0\u03bcg of lipid\u2010free human apoA\u2010I 3 times a week, while the other subset received 200\u00a0\u03bcg of albumin, as a control. Mice treated with lipid\u2010free apoA\u2010I showed a decrease in cholesterol deposition and immune cell retention in the aortic root compared with albumin\u2010treated mice, regardless of genotype. This reduction in atherosclerosis appeared to be directly related to a decrease in the number of\n              <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n              131 expressing cells and the esterified cholesterol to total cholesterol content in several immune cell compartments. In addition, apoA\u2010I treatment altered microdomain cholesterol composition that shifted\n              <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n              131, the common \u03b2 subunit of the interleukin 3 receptor, from lipid raft to nonraft fractions of the plasma membrane.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">ApoA\u2010I treatment reduced lipid and immune cell accumulation within the aortic root by systemically reducing microdomain cholesterol content in immune cells. These data suggest that lipid\u2010free apoA\u2010I mediates beneficial effects through attenuation of immune cell lipid raft cholesterol content, which affects numerous types of signal transduction pathways that rely on microdomain integrity for assembly and activation.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.116.004401","type":"journal-article","created":{"date-parts":[[2016,11,8]],"date-time":"2016-11-08T03:43:49Z","timestamp":1478576629000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":20,"title":["Lipid\u2010Free Apolipoprotein A\u2010I Reduces Progression of Atherosclerosis by Mobilizing Microdomain Cholesterol and Attenuating the Number of CD131 Expressing Cells: Monitoring Cholesterol Homeostasis Using the Cellular Ester to Total Cholesterol Ratio"],"prefix":"10.1161","volume":"5","author":[{"given":"Sushma","family":"Kaul","sequence":"first","affiliation":[{"name":"Department of Medicine, Medical 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