{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,30]],"date-time":"2025-10-30T17:22:48Z","timestamp":1761844968754,"version":"3.41.2"},"reference-count":54,"publisher":"Portland Press Ltd.","issue":"2","license":[{"start":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:00:00Z","timestamp":1567987200000},"content-version":"vor","delay-in-days":220,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2019,2,28]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Atherosclerosis is characterized by the accumulation of lipid-rich plaques in the arterial wall. Its pathogenesis is very complicated and has not yet been fully elucidated. It is known that dyslipidemia is a major factor in atherosclerosis. Several different Hermansky\u2013Pudlak syndrome (HPS) mutant mice have been shown either anti-atherosclerotic or atherogenic phenotypes, which may be mainly attributed to corresponding lipid perturbation. To explore the effects of different HPS proteins on lipid metabolism and plasma lipid composition, we analyzed the plasma lipid profiles of three HPS mutant mice, pa (Hps9\u2212\/\u2212), ru (Hps6\u2212\/\u2212), ep (Hps1\u2212\/\u2212), and wild-type (WT) mice. In pa and ru mice, some pro-atherosclerotic lipids, e.g. ceramide (Cer) and diacylglycerol (DAG), were down-regulated whereas triacylglycerol (TAG) containing docosahexaenoic acid (DHA) (22:6) fatty acyl was up-regulated when compared with WT mice. Several pro-atherosclerotic lipids including phosphatidic acid (PA), lysophosphatidylserine (LPS), sphingomyelin (SM), and cholesterol (Cho) were up-regulated in ep mice compared with WT mice. The lipid droplets in hepatocytes showed corresponding changes in these mutants. Our data suggest that the pa mutant resembles the ru mutant in its anti-atherosclerotic effects, but the ep mutant has an atherogenic effect. Our findings may provide clues to explain why different HPS mutant mice exhibit distinct anti-atherosclerotic or atherogenic effects after being exposed to high-cholesterol diets.<\/jats:p>","DOI":"10.1042\/bsr20182339","type":"journal-article","created":{"date-parts":[[2019,2,1]],"date-time":"2019-02-01T16:56:54Z","timestamp":1549040214000},"update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Plasma lipidomic profiling in murine mutants of Hermansky\u2013Pudlak syndrome reveals differential changes in pro- and anti-atherosclerotic lipids"],"prefix":"10.1042","volume":"39","author":[{"given":"Jing","family":"Ma","sequence":"first","affiliation":[{"name":"Beijing Key Laboratory for Genetics of Birth Defects, Beijing Pediatric Research Institute; Genetics and Birth Defects Control Center, National Center for Children\u2019s Health; MOE Key Laboratory of Major Diseases in Children; Beijing Children\u2019s Hospital, Capital Medical University, Beijing 100045, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Raoxu","family":"Wang","sequence":"additional","affiliation":[{"name":"Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sin\u00a0Man","family":"Lam","sequence":"additional","affiliation":[{"name":"Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chang","family":"Zhang","sequence":"additional","affiliation":[{"name":"Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Guanghou","family":"Shui","sequence":"additional","affiliation":[{"name":"Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7430-6019","authenticated-orcid":false,"given":"Wei","family":"Li","sequence":"additional","affiliation":[{"name":"Beijing Key Laboratory for Genetics of Birth Defects, Beijing Pediatric Research Institute; Genetics and Birth Defects Control Center, National Center for Children\u2019s Health; MOE Key Laboratory of Major Diseases in Children; Beijing Children\u2019s Hospital, Capital Medical University, Beijing 100045, China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"288","published-online":{"date-parts":[[2019,2,19]]},"reference":[{"key":"2021111619303062500_B1","doi-asserted-by":"publisher","first-page":"341","DOI":"10.1016\/j.cell.2011.04.005","article-title":"Macrophages in the pathogenesis of atherosclerosis","volume":"145","author":"Moore","year":"2011","journal-title":"Cell"},{"key":"2021111619303062500_B2","doi-asserted-by":"publisher","first-page":"551","DOI":"10.1161\/01.ATV.15.5.551","article-title":"The response-to-retention hypothesis of early atherogenesis","volume":"15","author":"Williams","year":"1995","journal-title":"Arterioscler. 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