June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Serum lipidomic analysis showed a dysregulation of sphingolipids in AMD patients, which may reflect the response of cells to lipid peroxidation products
Author Affiliations & Notes
  • Luciana Pujol-Lereis
    Institute of Human Genetics, University of Regensburg, Regensburg, Bayern, Germany
  • Gerhard Liebisch
    Institute of Clinical Chemistry and Laboratory Medicine, University of Regensburg , Regensburg, Bayern, Germany
  • Tina Schick
    Department of Ophthalmology, University Hospital of Cologne, Cologne, Germany
  • Sascha Fauser
    Department of Ophthalmology, University Hospital of Cologne, Cologne, Germany
  • Felix Graßmann
    Institute of Human Genetics, University of Regensburg, Regensburg, Bayern, Germany
  • Bernhard HF Weber
    Institute of Human Genetics, University of Regensburg, Regensburg, Bayern, Germany
  • Footnotes
    Commercial Relationships   Luciana Pujol-Lereis, None; Gerhard Liebisch, None; Tina Schick, None; Sascha Fauser, None; Felix Graßmann, None; Bernhard Weber, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 5230. doi:
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      Luciana Pujol-Lereis, Gerhard Liebisch, Tina Schick, Sascha Fauser, Felix Graßmann, Bernhard HF Weber; Serum lipidomic analysis showed a dysregulation of sphingolipids in AMD patients, which may reflect the response of cells to lipid peroxidation products. Invest. Ophthalmol. Vis. Sci. 2017;58(8):5230.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : Lipid related-genes, accumulation of lipids in drusen and high density lipoprotein (HDL) levels have been associated with age-related macular degeneration (AMD), although analyses of serum total fatty acids, cholesterol, triglycerides, and phospholipids in patients provided no further supporting evidence. To search for novel lipid biomarkers in AMD, we measured serum lipid species from lipid classes associated with inflammation and oxidative stress. In addition, we evaluated the effects of malondialdehyde-acetaldehyde (MAA) adducts in the gene regulation of lipid metabolism in retinal cell lines.

Methods : Serum samples of healthy controls (n=129) and AMD patients with geographic atrophy (GA, n=47) and choroidal neovascularization (CNV, n=197) were used. Lipids were extracted according to the Bligh and Dyer method, and lipid species were quantified by electrospray ionization tandem mass spectrometry. Statistical significance was determined by linear regression adjusted for age, gender and batch, with corrections for multiple comparisons within each lipid class. Weri Rb-1 and ARPE-19 cells were incubated with MAA-BSA or BSA (n=6). RNA was extracted and quantitative PCR performed with the Universal Probe Library from Roche and Taqman reagents. Expression data was analyzed using paired t-tests.

Results : We found four lipid species with a significant increase in AMD patients compared to controls (Hexocylceramide d18:1/16:0, p=0.008; Phosphatidylcholines PC O-38:5, PC O-38:4, PC O-40:6, all with p=0.049), and two lipid species with higher levels specifically for GA (Ceramide d18:1/16:0, p=0.037) or CNV (Cholesteryl ester 18:0, p=0.027). Also, for Weri Rb-1 cells we found an upregulated expression of genes in the ceramide metabolism under MAA-BSA treatment, specifically for SPTLC1, DEGS1, CERS2, CERS6 and UGCG (all p<0.001). For ARPE-19 cells, we observed a decrease in the expression of SMPD2 and SMPD3 with MAA-BSA addition (both p<0.05). The latter finding implies a downregulation of genes involved in the synthesis of sphingomyelin from ceramides, while the former data point to an upregulation of ceramide and glucosylceramide synthesis pathways.

Conclusions : Specific lipid species were found to be significantly altered in AMD patients. Moreover, our findings suggest that dysregulation of sphingolipid metabolism may play a role in AMD etiology.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.

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