June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Amyloid Beta 1- 42 Promotes NLRP3-inflammasome Activation In Retinal Pigmented Epithelial Cells
Author Affiliations & Notes
  • Matthew West
    Department of Ophthalmology, Georgia Health Sciences University, Augusta, GA
  • Folami Lamoke
    Department of Ophthalmology, Georgia Health Sciences University, Augusta, GA
  • AnnaLisa Montemari
    Department of Experimental Medicine and Pathology, University of Rome, Rome, Italy
  • Giovanni Parisi
    IRCCS Fondazione GB Bietti, Rome, Italy
  • Guido Ripandelli
    IRCCS Fondazione GB Bietti, Rome, Italy
  • Dennis Marcus
    Southeast Retina Center, Augusta, GA
  • Manuela Bartoli
    Department of Ophthalmology, Georgia Health Sciences University, Augusta, GA
  • Footnotes
    Commercial Relationships Matthew West, None; Folami Lamoke, None; AnnaLisa Montemari, None; Giovanni Parisi, None; Guido Ripandelli, None; Dennis Marcus, Genentech (C), Genentech (F), Regeneron (F), Regeneron (C), Thrombogenics (F), Thrombogenics (C), Allergan (F), Pfizer (F), Santen (F), Alimera (F), LPath (F), Acucela (F), Galaxo Smith Kline (F); Manuela Bartoli, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 4994. doi:
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    • Get Citation

      Matthew West, Folami Lamoke, AnnaLisa Montemari, Giovanni Parisi, Guido Ripandelli, Dennis Marcus, Manuela Bartoli; Amyloid Beta 1- 42 Promotes NLRP3-inflammasome Activation In Retinal Pigmented Epithelial Cells. Invest. Ophthalmol. Vis. Sci. 2013;54(15):4994.

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

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Abstract
 
Purpose
 

Accumulation of amyloid beta peptides (A-beta) has been shown to be a potential contributing factor for the development of age-related macular degeneration (AMD). Recent work has shed light on the role of the pro-inflammatory macromolecular complex of the NLRP3-inflammasome in the pathogenesis of geographical atrophy (GA). Our previous studies have shown that A-beta increases the expression of the thioredoxin-interacting protein (TXNIP), a constituent of the NLRP3-inflammasome complex. In this study we wanted to determine whether A-beta stimulation of retinal pigmented epithelial cells (ARPE19) promoted the expression, activation and protein-protein interaction of constituents of the NLRP3-inflammasome.

 
Methods
 

Human retinal pigmented epithelial cells (ARPE19) were stimulated for 24 hours with 10μM of A-beta 1-42 or 10μM of the reverse peptide A-beta 42-1, which was used as control. Western blotting and immunoprecipitation analyses were performed to determine the expression and protein-protein interaction of the inflammasome constituent TLR4, NLRP3, ASC and TXNIP and to determine the expression of A-beta receptor (RAGE). NLRP3-activation was determined by measuring caspase1 activity. RAGE inhibition was achieved by transfecting ARPE19 with specific siRNA.

 
Results
 

A-beta treatment of ARPE19 promoted the expression of RAGE, TLR4, NLRP3 and TXNIP. Immunocytochemistry revealed that A-beta stimulated NLRP3 interaction with ASC and TXNIP and this effect was followed by increased caspase1 activity. Selective blockade of RAGE, by RNA silencing, blocked A-beta -induced activation of NLRP3-inflammasome in ARPE19, as assessed by monitoring caspase 1 activity.

 
Conclusions
 

The specific role of A-beta in the pathogenesis of wet AMD or GA is still controversial. Our data demonstrating that A-beta can promote RPE cells damage by inducing the NLRP3-inflammasome, further confirm a clear role of A-beta in the early pathogenesis of AMD.

 
Keywords: 412 age-related macular degeneration • 701 retinal pigment epithelium • 557 inflammation  
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