title: Human smooth muscle cell subpopulations differentially accumulate cholesteryl ester when exposed to native and oxidized lipoproteins.
abstract: BACKGROUND
  Vascular smooth muscle cells (SMCs) manifest diverse phenotypes and emerging evidence suggests this is caused by inherently distinct SMC subtypes. Recently, Li et al (Circ Res 2001;89:517-525) successfully cloned 2 uniquely responsive SMC subpopulations from a single human artery and we used this unique resource to test the hypothesis that distinct SMC subtypes are differential precursors of foam cell formation.
  
  
  RESULTS
  When challenged with human atherogenic native or oxidized hypertriglyceridemic very-low-density lipoprotein (HTG-VLDL), the larger, slower-growing, spindle-shaped HITB5 SMC clone accumulated significantly more cholesteryl ester (CE) and triglyceride (TG) than the smaller, faster-growing epithelioid-shaped HITA2 SMC clone (10 versus 2 microg CE/mg cell protein [PN] and 60 versus 7 microg TG/mg PN, P<0.05). Lipoprotein lipase (LPL), a key enzyme involved in lipoprotein uptake, was identified as one differentially expressed protein that altered the predisposition of HITA2 SMCs for lipid accumulation. Although HITB5 SMCs secreted significantly more LPL than did HITA2 SMCs (0.7 versus 0.2 U/mL media, P<0.05), the addition of bovine milk LPL to HITA2 SMCs, significantly increased native and oxidized HTG-VLDL-induced lipid accumulation.
  
  
  CONCLUSIONS
  Inherently distinct SMC subsets are differentially predisposed to lipoprotein-induced lipid accumulation. Moreover, the environment can influence the response of SMC subsets to atherogenic lipoproteins.
authors.affiliation: Vascular Biology Group at the Robarts Research Institute, University of Western Ontario, London, Ontario, Canada.
authors.forename: Carmen A
authors.initials: CA
authors.lastname: Argmann
authors.forename: Cynthia G
authors.initials: CG
authors.lastname: Sawyez
authors.forename: Shaohua
authors.initials: S
authors.lastname: Li
authors.forename: Zengxuan
authors.initials: Z
authors.lastname: Nong
authors.forename: Robert A
authors.initials: RA
authors.lastname: Hegele
authors.forename: J Geoffrey
authors.initials: JG
authors.lastname: Pickering
authors.forename: Murray W
authors.initials: MW
authors.lastname: Huff
mesh_terms: D000818:Animals; D001161:Arteriosclerosis / Q000097:blood; D001391:Azo Compounds; D002417:Cattle; D002454:Cell Differentiation; D048430:Cell Shape / Q000187:drug effects; D002478:Cells, Cultured / Q000187:drug effects / Q000378:metabolism; D002788:Cholesterol Esters / Q000378:metabolism*; D002999:Clone Cells / Q000187:drug effects / Q000378:metabolism; D004396:Coloring Agents; D004198:Disease Susceptibility; D005487:Foam Cells / Q000378:metabolism*; D006801:Humans; D015228:Hypertriglyceridemia / Q000097:blood; D008071:Lipoprotein Lipase / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000494:pharmacology*; D008079:Lipoproteins, VLDL / Q000494:pharmacology*; D008894:Milk Proteins / Q000494:pharmacology; D009131:Muscle, Smooth, Vascular / Q000166:cytology* / Q000378:metabolism; D032389:Myocytes, Smooth Muscle / Q000145:classification / Q000187:drug effects* / Q000378:metabolism; D002785:Sterol O-Acyltransferase / Q000378:metabolism; D014280:Triglycerides / Q000378:metabolism
chemical_list: D001391:Azo Compounds; D002788:Cholesterol Esters; D004396:Coloring Agents; D008077:Lipoproteins, LDL; D008079:Lipoproteins, VLDL; D008894:Milk Proteins; D014280:Triglycerides; C032629:acetyl-LDL; C099252:oxidized low density lipoprotein; D002785:Sterol O-Acyltransferase; D008071:Lipoprotein Lipase; C011049:oil red O