title: High-Density Lipoprotein Function in Exudative Age-Related Macular Degeneration.
abstract: High-density lipoproteins (HDL) have long been implicated in the pathogenesis of age-related macular degeneration (AMD). However, conflicting results have been reported with regard to the associations of AMD with HDL-cholesterol levels. The present study is the first to assess HDL composition and metrics of HDL function in patients with exudative AMD and control patients.
  
  
  
  Blood samples were collected from 29 patients with exudative AMD and 26 age-matched control patients. Major HDL associated apolipoproteins were determined in apoB-depleted serum by immunoturbidimetry or ELISA, HDL-associated lipids were quantified enzymatically. To get an integrated measure of HDL quantity and quality, we assessed several metrics of HDL function, including cholesterol efflux capacity, anti-oxidative and anti-inflammatory activities using apoB-depleted serum from study participants.
  
  
  
  In our study, we observed that the HDL associated acute phase protein serum amyloid A (SAA) was significantly increased in AMD patients (p<0.01), whereas all other assessed apolipoproteins including ApoA-I, apoA-II, apoC-II, apoC-III and apoE as well as major HDL associated lipids were not altered. HDL efflux capacity, anti-oxidative capacity and arylesterase activity were not different in AMD patients when compared with the control group. The ability of apoB-depleted serum to inhibit monocyte NF-κB expression was significantly improved in AMD patients (mean difference (MD) -5.6, p<0.01). Moreover, lipoprotein-associated phospholipase A2 activity, a marker of vascular inflammation, was decreased in AMD subjects (MD -24.1, p<0.01).
  
  
  
  The investigated metrics of HDL composition and HDL function were not associated with exudative AMD in this study, despite an increased content of HDL associated SAA in AMD patients. Unexpectedly, anti-inflammatory activity of apoB-depleted serum was even increased in our study. Our data suggest that the investigated parameters of serum HDL function showed no significant association with exudative AMD. However, we cannot exclude that alterations in locally produced HDL may be part of the AMD pathogenesis.
authors.affiliation: Department of Ophthalmology, Medical University of Graz, Graz, Austria.
authors.forename: Laura
authors.initials: L
authors.lastname: Pertl
authors.affiliation: Institute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria.
authors.forename: Sabine
authors.initials: S
authors.lastname: Kern
authors.affiliation: Department of Ophthalmology, Medical University of Graz, Graz, Austria.
authors.forename: Martin
authors.initials: M
authors.lastname: Weger
authors.affiliation: Department of Ophthalmology, Medical University of Graz, Graz, Austria.
authors.forename: Silke
authors.initials: S
authors.lastname: Hausberger
authors.affiliation: Institute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria.
authors.forename: Markus
authors.initials: M
authors.lastname: Trieb
authors.affiliation: Department of Ophthalmology, Medical University of Graz, Graz, Austria.
authors.forename: Vanessa
authors.initials: V
authors.lastname: Gasser-Steiner
authors.affiliation: Department of Ophthalmology, Medical University of Graz, Graz, Austria.
authors.forename: Anton
authors.initials: A
authors.lastname: Haas
authors.affiliation: Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Graz, Austria.
authors.forename: Hubert
authors.initials: H
authors.lastname: Scharnagl
authors.affiliation: Institute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria.
authors.forename: Akos
authors.initials: A
authors.lastname: Heinemann
authors.affiliation: Institute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria.
authors.forename: Gunther
authors.initials: G
authors.lastname: Marsche
mesh_terms: D000368:Aged; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D000975:Antioxidants / Q000378:metabolism; D043303:Aryldialkylphosphatase / Q000378:metabolism; D002784:Cholesterol / Q000378:metabolism; D003710:Demography; D006801:Humans; D008075:Lipoproteins, HDL / Q000097:blood*; D051379:Mice; D010084:Oxidation-Reduction; D054467:Phospholipases A2 / Q000378:metabolism; D000067996:RAW 264.7 Cells; D000685:Serum Amyloid A Protein / Q000378:metabolism; D057135:Wet Macular Degeneration / Q000097:blood*
chemical_list: D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D008075:Lipoproteins, HDL; D000685:Serum Amyloid A Protein; D002784:Cholesterol; D054467:Phospholipases A2; D043303:Aryldialkylphosphatase