{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T16:02:15Z","timestamp":1779120135460,"version":"3.51.4"},"reference-count":36,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"13","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2019,7,2]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Micro\n              <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n              (miR)\u201033 targets cholesterol transporter\n              <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>\n              \u2010binding cassette protein A1 and other antiatherogenic targets and contributes to atherogenic progression. Its inhibition or deletion is known to result in the amelioration of atherosclerosis in mice. However, mice lack the other member of the miR\u201033 family, miR\u201033b, which exists in humans and other large mammals. Thus, precise evaluation and comparison of the responsibilities of these 2 miRs during the progression of atherosclerosis has not been reported, although they are essential.\n            <\/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              In this study, we performed a comprehensive analysis of the difference between the function of miR\u201033a and miR\u201033b using genetically modified mice. We generated 4 strains with or without miR\u201033a and miR\u201033b. Comparison between mice with only miR\u201033a (wild\u2010type mice) and mice with only miR\u201033b (miR\u201033a\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              \/miR\u201033b\n              <jats:sup>+\/+<\/jats:sup>\n              ) revealed the dominant expression of miR\u201033b in the liver. To evaluate the whole body atherogenic potency of miR\u201033a and miR\u201033b, we developed apolipoprotein E\u2013deficient\/miR\u201033a\n              <jats:sup>+\/+<\/jats:sup>\n              \/miR\u201033b\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice and apolipoprotein E\u2013deficient\/miR\u201033a\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              \/miR\u201033b\n              <jats:sup>+\/+<\/jats:sup>\n              mice. With a high\u2010fat and high\u2010cholesterol diet, the apolipoprotein E\u2013deficient\/miR\u201033a\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              \/miR\u201033b\n              <jats:sup>+\/+<\/jats:sup>\n              mice developed increased atherosclerotic plaque versus apolipoprotein E\u2013deficient\/miR\u201033a\n              <jats:sup>+\/+<\/jats:sup>\n              \/miR\u201033b\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice, in line with the predominant expression of miR\u201033b in the liver and worsened serum cholesterol profile. By contrast, a bone marrow transplantation study showed no significant difference, which was consistent with the relevant expression levels of miR\u201033a and miR\u201033b in bone marrow cells.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">The miR\u201033 family exhibits differences in distribution and regulation and particularly in the progression of atherosclerosis; miR\u201033b would be more potent than miR\u201033a.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.119.012609","type":"journal-article","created":{"date-parts":[[2019,6,27]],"date-time":"2019-06-27T09:06:06Z","timestamp":1561626366000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":23,"title":["Identification of Differential Roles of MicroRNA\u201033a and \u201033b During Atherosclerosis Progression With Genetically Modified 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