{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,13]],"date-time":"2026-01-13T00:51:07Z","timestamp":1768265467857,"version":"3.49.0"},"reference-count":45,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2018,7]]},"abstract":"<jats:sec>\n            <jats:title>Objective\u2014<\/jats:title>\n            <jats:p>Reverse cholesterol transport (RCT) is a major mechanism by which HDL (high-density lipoprotein) protects against atherosclerosis. Endothelial lipase (EL) reportedly reduces HDL levels, which, in theory, would increase atherosclerosis. However, it remains unclear whether EL affects RCT in vivo.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results\u2014<\/jats:title>\n            <jats:p>\n              Adenoviral vectors expressing EL or luciferase were intravenously injected into mice, and a macrophage RCT assay was performed. As expected, hepatic EL overexpression markedly reduced HDL levels. In parallel, plasma\n              <jats:sup>3<\/jats:sup>\n              H-cholesterol counts from the EL-expressing mice decreased by 85% compared with control. Surprisingly, there was no difference in fecal\n              <jats:sup>3<\/jats:sup>\n              H-cholesterol excretion between the groups. Kinetic studies revealed increased catabolism\/hepatic uptake of\n              <jats:sup>3<\/jats:sup>\n              HDL-cholesteryl ether, resulting in no change in fecal HDL-cholesteryl ester excretion in the mice. To explore underlying mechanisms for the preservation of RCT despite low HDL levels in the EL-expressing mice, we investigated the effects of hepatic SR-BI (scavenger receptor class B type I) knockdown. RCT assay revealed that knockdown of SR-BI alone reduced fecal excretion of macrophage-derived\n              <jats:sup>3<\/jats:sup>\n              H-cholesterol. Interestingly, hepatic EL overexpression under SR-BI inhibition further attenuated fecal tracer counts as compared with control. Finally, we observed that EL overexpression enhanced in vivo RCT under pharmacological inhibition of hepatic ABCA1 (ATP-binding cassette transporter A1) by probucol.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions\u2014<\/jats:title>\n            <jats:p>Hepatic EL expression compensates for reduced macrophage-derived cholesterol efflux to plasma because of low HDL levels by promoting cholesterol excretion to bile\/feces via an SR-BI pathway, maintaining overall RCT in vivo. In contrast, EL-modified HDL might negatively regulate RCT via hepatic ABCA1. Despite extreme hypoalphalipoproteinemia, RCT is maintained in EL-expressing mice via SR-BI\/ABCA1-dependent pathways.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.118.311056","type":"journal-article","created":{"date-parts":[[2018,5,10]],"date-time":"2018-05-10T09:00:13Z","timestamp":1525942813000},"page":"1454-1467","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":25,"title":["Hepatic Overexpression of Endothelial Lipase Lowers High-Density Lipoprotein but Maintains Reverse Cholesterol Transport in Mice"],"prefix":"10.1161","volume":"38","author":[{"given":"Shunichi","family":"Takiguchi","sequence":"first","affiliation":[{"name":"From the Division of Anti-Aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan (S.T., M.A., E.Y., T.N., K.N., M.S., M.I., H.U.-K., Y.T., M.Y., T.K., K.I.)"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Makoto","family":"Ayaori","sequence":"additional","affiliation":[{"name":"From the Division of Anti-Aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan (S.T., M.A., E.Y., T.N., K.N., M.S., M.I., H.U.-K., Y.T., M.Y., T.K., K.I.)"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Emi","family":"Yakushiji","sequence":"additional","affiliation":[{"name":"From the Division of Anti-Aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan (S.T., M.A., E.Y., T.N., K.N., M.S., M.I., H.U.-K., Y.T., M.Y., T.K., K.I.)"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takafumi","family":"Nishida","sequence":"additional","affiliation":[{"name":"From the Division of Anti-Aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan (S.T., M.A., E.Y., T.N., K.N., M.S., M.I., H.U.-K., Y.T., M.Y., T.K., K.I.)"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kazuhiro","family":"Nakaya","sequence":"additional","affiliation":[{"name":"From the Division of Anti-Aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan (S.T., M.A., E.Y., T.N., K.N., M.S., M.I., H.U.-K., Y.T., M.Y., T.K., K.I.)"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Makoto","family":"Sasaki","sequence":"additional","affiliation":[{"name":"From the Division of Anti-Aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan (S.T., M.A., E.Y., T.N., K.N., M.S., M.I., H.U.-K., Y.T., M.Y., T.K., K.I.)"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maki","family":"Iizuka","sequence":"additional","affiliation":[{"name":"From the Division of Anti-Aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan (S.T., M.A., E.Y., T.N., K.N., M.S., M.I., H.U.-K., Y.T., M.Y., T.K., K.I.)"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Harumi","family":"Uto-Kondo","sequence":"additional","affiliation":[{"name":"From the Division of Anti-Aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan (S.T., M.A., E.Y., T.N., K.N., M.S., M.I., H.U.-K., Y.T., M.Y., T.K., K.I.)"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yoshio","family":"Terao","sequence":"additional","affiliation":[{"name":"From the Division of Anti-Aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan (S.T., M.A., E.Y., T.N., K.N., M.S., M.I., H.U.-K., Y.T., M.Y., T.K., K.I.)"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Makiko","family":"Yogo","sequence":"additional","affiliation":[{"name":"From the Division of Anti-Aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan (S.T., M.A., E.Y., T.N., K.N., M.S., M.I., H.U.-K., Y.T., M.Y., T.K., K.I.)"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tomohiro","family":"Komatsu","sequence":"additional","affiliation":[{"name":"From the Division of Anti-Aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan (S.T., M.A., E.Y., T.N., K.N., M.S., M.I., H.U.-K., Y.T., M.Y., T.K., K.I.)"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masatsune","family":"Ogura","sequence":"additional","affiliation":[{"name":"Department of Molecular Innovation in Lipidology, National Cerebral and Cardiovascular Center, Osaka, Japan (M.O.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Katsunori","family":"Ikewaki","sequence":"additional","affiliation":[{"name":"From the Division of Anti-Aging 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