title: Lipoprotein lipase in aortic valve stenosis is associated with lipid retention and remodelling.
abstract: BACKGROUND
  Calcific aortic valve disease (CAVD) is a chronic disorder characterized by a fibrocalcific remodelling. It is suspected that lipid retention within the aortic valve may be one important mechanism participating to aortic valve remodelling. Lipoprotein lipase (LPL) is implicated in lipid metabolism and may play a role in lipid retention within the aortic valve.
  
  
  METHODS
  In 57 patients, CAVD were analysed for the expression of LPL by q-PCR and immunohistochemistry. Expression of oxidized-LDL (ox-LDL) and decorin was also documented. In addition, a complete blood profile, including the size of LDL and high-density lipoprotein (HDL) particles, were performed to find associations between the blood lipid profile and expression of ox-LDL and LPL within CAVD.
  
  
  RESULTS
  Immunohistochemistry studies revealed that LPL was expressed in stenotic aortic valves as a diffuse staining and also in dense cellular areas where macrophages were abundant. Expression of LPL co-localized with decorin and ox-LDL. In turn, valves with higher amount of ox-LDL had elevated number of LPL transcripts. In addition, we documented that the small, dense HDL phenotype was associated with an elevated amount of ox-LDL and LPL transcripts within CAVD. Furthermore, expression of LPL was associated with several indices of fibrocalcific remodelling of the aortic valve.
  
  
  CONCLUSIONS
  Expression of LPL within CAVD is related to the amount of ox-LDL, which is, in turn, associated with the small, dense HDL phenotype. Lipid retention associated with smaller HDL particles may participate in the expression of LPL, whereby a fibrocalcific remodelling of the aortic valve is promoted.
authors.affiliation: Department of Surgery, Laboratoire d'Études Moléculaires des Valvulopathies, Groupe de Recherche en Valvulopathies, Quebec Heart and Lung Institute/Research Center, Laval University, Quebec City, QC, Canada.
authors.forename: Ablajan
authors.initials: A
authors.lastname: Mahmut
authors.forename: Marie-Chloé
authors.initials: MC
authors.lastname: Boulanger
authors.forename: Dominique
authors.initials: D
authors.lastname: Fournier
authors.forename: Christian
authors.initials: C
authors.lastname: Couture
authors.forename: Sylvain
authors.initials: S
authors.lastname: Trahan
authors.forename: Sylvain
authors.initials: S
authors.lastname: Pagé
authors.forename: Benoît
authors.initials: B
authors.lastname: Arsenault
authors.forename: Jean-Pierre
authors.initials: JP
authors.lastname: Després
authors.forename: Philippe
authors.initials: P
authors.lastname: Pibarot
authors.forename: Patrick
authors.initials: P
authors.lastname: Mathieu
mesh_terms: D000368:Aged; D001021:Aortic Valve / Q000201:enzymology / Q000473:pathology*; D001024:Aortic Valve Stenosis / Q000201:enzymology* / Q000473:pathology; D005260:Female; D005355:Fibrosis / Q000201:enzymology; D006801:Humans; D007150:Immunohistochemistry; D008071:Lipoprotein Lipase / Q000378:metabolism*; D008075:Lipoproteins, HDL / Q000378:metabolism*; D008077:Lipoproteins, LDL / Q000378:metabolism*; D008297:Male; D061205:Vascular Calcification / Q000201:enzymology* / Q000473:pathology
chemical_list: D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D008071:Lipoprotein Lipase