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Adiponectin Mediates Dietary Omega-3 Long-Chain Polyunsaturated Fatty Acid Protection Against Choroidal Neovascularization in Mice.

Abstract Neovascular age-related macular degeneration (AMD) is a major cause of legal blindness in the elderly. Diets with omega3-long-chain-polyunsaturated-fatty-acid (ω3-LCPUFA) correlate with a decreased risk of AMD. Dietary ω3-LCPUFA versus ω6-LCPUFA inhibits mouse ocular neovascularization, but the underlying mechanism needs further exploration. The aim of this study was to investigate if adiponectin (APN) mediated ω3-LCPUFA suppression of neovessels in AMD.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title investigative ophthalmology & visual science
Publication Year Start




PMID- 28763559
OWN - NLM
STAT- MEDLINE
DA  - 20170801
DCOM- 20170803
LR  - 20170805
IS  - 1552-5783 (Electronic)
IS  - 0146-0404 (Linking)
VI  - 58
IP  - 10
DP  - 2017 Aug 01
TI  - Adiponectin Mediates Dietary Omega-3 Long-Chain Polyunsaturated Fatty Acid
      Protection Against Choroidal Neovascularization in Mice.
PG  - 3862-3870
LID - 10.1167/iovs.17-21796 [doi]
AB  - Purpose: Neovascular age-related macular degeneration (AMD) is a major cause of
      legal blindness in the elderly. Diets with
      omega3-long-chain-polyunsaturated-fatty-acid (omega3-LCPUFA) correlate with a
      decreased risk of AMD. Dietary omega3-LCPUFA versus omega6-LCPUFA inhibits mouse 
      ocular neovascularization, but the underlying mechanism needs further
      exploration. The aim of this study was to investigate if adiponectin (APN)
      mediated omega3-LCPUFA suppression of neovessels in AMD. Methods: The mouse
      laser-induced choroidal neovascularization (CNV) model was used to mimic some of 
      the inflammatory aspect of AMD. CNV was compared between wild-type (WT) and
      Apn-/- mice fed either otherwise matched diets with 2% omega3 or 2%
      omega6-LCPUFAs. Vldlr-/- mice were used to mimic some of the metabolic aspects of
      AMD. Choroid assay ex vivo and human retinal microvascular endothelial cell
      (HRMEC) proliferation assay in vitro was used to investigate the APN pathway in
      angiogenesis. Western blot for p-AMPKalpha/AMPKalpha and qPCR for Apn, Mmps, and 
      IL-10 were used to define mechanism. Results: omega3-LCPUFA intake suppressed
      laser-induced CNV in WT mice; suppression was abolished with APN deficiency.
      omega3-LCPUFA, mediated by APN, decreased mouse Mmps expression. APN deficiency
      decreased AMPKalpha phosphorylation in vivo and exacerbated choroid-sprouting ex 
      vivo. APN pathway activation inhibited HRMEC proliferation and decreased Mmps. In
      Vldlr-/- mice, omega3-LCPUFA increased retinal AdipoR1 and inhibited NV.
      omega3-LCPUFA decreased IL-10 but did not affect Mmps in Vldlr-/- retinas.
      Conclusions: APN in part mediated omega3-LCPUFA inhibition of neovascularization 
      in two mouse models of AMD. Modulating the APN pathway in conjunction with a
      omega3-LCPUFA-enriched-diet may augment the beneficial effects of omega3-LCPUFA
      in AMD patients.
FAU - Fu, Zhongjie
AU  - Fu Z
AD  - Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, 
      Boston, Massachusetts, United States.
FAU - Liegl, Raffael
AU  - Liegl R
AD  - Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, 
      Boston, Massachusetts, United States.
FAU - Wang, Zhongxiao
AU  - Wang Z
AD  - Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, 
      Boston, Massachusetts, United States.
FAU - Gong, Yan
AU  - Gong Y
AD  - Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, 
      Boston, Massachusetts, United States.
FAU - Liu, Chi-Hsiu
AU  - Liu CH
AD  - Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, 
      Boston, Massachusetts, United States.
FAU - Sun, Ye
AU  - Sun Y
AD  - Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, 
      Boston, Massachusetts, United States.
FAU - Cakir, Bertan
AU  - Cakir B
AD  - Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, 
      Boston, Massachusetts, United States.
FAU - Burnim, Samuel B
AU  - Burnim SB
AD  - Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, 
      Boston, Massachusetts, United States.
FAU - Meng, Steven S
AU  - Meng SS
AD  - Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, 
      Boston, Massachusetts, United States.
FAU - Lofqvist, Chatarina
AU  - Lofqvist C
AD  - Department of Ophthalmology, Sahlgrenska Academy at University of Gothenburg,
      Gothenburg, Sweden.
FAU - SanGiovanni, John Paul
AU  - SanGiovanni JP
AD  - National Institute on Alcohol Abuse and Alcoholism, National Institutes of
      Health, Bethesda, Maryland, and Georgetown University School of Medicine,
      Washington, District of Columbia, United States.
FAU - Hellstrom, Ann
AU  - Hellstrom A
AD  - Department of Ophthalmology, Sahlgrenska Academy at University of Gothenburg,
      Gothenburg, Sweden.
FAU - Smith, Lois E H
AU  - Smith LEH
AD  - Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, 
      Boston, Massachusetts, United States.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Invest Ophthalmol Vis Sci
JT  - Investigative ophthalmology & visual science
JID - 7703701
RN  - 0 (Adiponectin)
RN  - 0 (Biomarkers)
RN  - 0 (Fatty Acids, Omega-3)
RN  - 0 (Receptors, Adiponectin)
RN  - EC 3.4.24.- (Matrix Metalloproteinases)
SB  - IM
MH  - Adiponectin/*physiology
MH  - Animals
MH  - Biomarkers/metabolism
MH  - Blotting, Western
MH  - Cell Proliferation/drug effects
MH  - Choroidal Neovascularization/metabolism/*prevention & control
MH  - Disease Models, Animal
MH  - Endothelial Cells/drug effects
MH  - Fatty Acids, Omega-3/*pharmacology
MH  - Macular Degeneration/*complications
MH  - Matrix Metalloproteinases/metabolism
MH  - Mice
MH  - Receptors, Adiponectin/metabolism
PMC - PMC5539800
EDAT- 2017/08/02 06:00
MHDA- 2017/08/05 06:00
CRDT- 2017/08/02 06:00
AID - 2646834 [pii]
AID - 10.1167/iovs.17-21796 [doi]
PST - ppublish
SO  - Invest Ophthalmol Vis Sci. 2017 Aug 1;58(10):3862-3870. doi:
      10.1167/iovs.17-21796.