title: Polyunsaturated fatty acid relatively decreases cholesterol content in THP-1 macrophage-derived foam cell: partly correlates with expression profile of CIDE and PAT members.
abstract: BACKGROUND
  Polyunsaturated fatty acids (PUFAs) have positive effect on the regulation of plasma lipids. But the mechanism for them to modulate lipid homeostasis in macrophage is still unclear. In this study, we employed PUFA to pretreat macrophages and evaluated the variations of lipid droplet (LD) content, lipid composition, and expressions of LD-associated genes in macrophage-derived foam cells.
  
  
  METHODS
  THP-1-derived macrophages or human peripheral blood monocyte-derived macrophages were pre-treated with four non-esterified fatty acids (NEFAs) separately: saturated fatty acid (SFA)-palmitic acid (PA), monounsaturated fatty acids (MUFAs)-oleic acid (OA), PUFAs-linoleic acid (LA) and eicosapentaenoic acid (EPA). Intracellular lipid content and cholesterol efflux were analyzed in THP-1 macrophage-derived foam cells. Related gene expressions were detected by quantitative real-time PCR.
  
  
  RESULTS
  PUFA pre-treatment reduced cholesterol content in foam cells and increased cholesterol efflux to lipid-free apoAI in conditioned medium compared with PA or OA group. Cell death-inducing DFF45 like effector (CIDE) and Perilipin-Adipophilin-TIP47 (PAT) family members, as LD-associated proteins, showed specific gene expression profiles after PUFA pre-treatment. These results may help to explain the process of lipid metabolism within foam cells.
  
  
  CONCLUSIONS
  PUFA (LA or EPA) had a potential protective effect against cholesterol accumulation. The specific expressions of CIDE and PAT genes may provide clues to explore the protective mechanism of PUFA in foam cells.
authors.affiliation: State Key Laboratory of Cancer Biology and Department of Pathology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
authors.forename: Yue
authors.initials: Y
authors.lastname: Song
authors.forename: Li-Jun
authors.initials: LJ
authors.lastname: Zhang
authors.forename: Hang
authors.initials: H
authors.lastname: Li
authors.forename: Yu
authors.initials: Y
authors.lastname: Gu
authors.forename: Fan-Fan
authors.initials: FF
authors.lastname: Li
authors.forename: Li-Na
authors.initials: LN
authors.lastname: Jiang
authors.forename: Fang
authors.initials: F
authors.lastname: Liu
authors.forename: Jing
authors.initials: J
authors.lastname: Ye
authors.forename: Qing
authors.initials: Q
authors.lastname: Li
mesh_terms: D000217:Acyltransferases / Q000096:biosynthesis*; D051017:Apoptosis Regulatory Proteins / Q000096:biosynthesis*; D050197:Atherosclerosis / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D002784:Cholesterol / Q000097:blood*; D015118:Eicosapentaenoic Acid / Q000008:administration & dosage; D005487:Foam Cells / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D019787:Linoleic Acid / Q000008:administration & dosage; D008055:Lipids / Q000097:blood / Q000235:genetics*; D008264:Macrophages / Q000187:drug effects; D019301:Oleic Acid / Q000008:administration & dosage; D019308:Palmitic Acid / Q000008:administration & dosage; D059467:Transcriptome / Q000187:drug effects
chemical_list: D051017:Apoptosis Regulatory Proteins; D008055:Lipids; D019301:Oleic Acid; D019308:Palmitic Acid; D002784:Cholesterol; D019787:Linoleic Acid; D015118:Eicosapentaenoic Acid; D000217:Acyltransferases; C105599:HHAT protein, human