September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
PROTECTIVE EFFECTS OF TGF-β1 AGAINST AMYLOID-β1-42 OLIGOMERS-INDUCED RETINAL DAMAGE
Author Affiliations & Notes
  • Claudio Bucolo
    Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy
  • Vincenzo Fisichella
    Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy
  • Giovanni Giurdanella
    Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy
  • Chiara Bianca Maria Platania
    Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy
  • Giovanni Luca Romano
    Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy
  • Federica Geraci
    Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy
  • Filippo Drago
    Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy
  • Footnotes
    Commercial Relationships   Claudio Bucolo, None; Vincenzo Fisichella, None; Giovanni Giurdanella, None; Chiara Bianca Maria Platania, None; Giovanni Luca Romano, None; Federica Geraci, None; Filippo Drago, None
  • Footnotes
    Support  none
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 119. doi:
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      Claudio Bucolo, Vincenzo Fisichella, Giovanni Giurdanella, Chiara Bianca Maria Platania, Giovanni Luca Romano, Federica Geraci, Filippo Drago; PROTECTIVE EFFECTS OF TGF-β1 AGAINST AMYLOID-β1-42 OLIGOMERS-INDUCED RETINAL DAMAGE. Invest. Ophthalmol. Vis. Sci. 2016;57(12):119.

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

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Abstract

Purpose : To set up a retinal neurodegenerative model in rat that mimics pathologic conditions such as age-related macular degeneration (AMD) using amyloid-β (Aβ) oligomers, and assess the effect of TGF-β1.

Methods : Sprague-Dawley male rats were used. Human Aβ1-42 oligomers were intravitreally (ITV) injected (10 µM) in the presence or in the absence of recombinant human TGF-β1 (1ng/ml ITV injected). After 48h, the animals were sacrificed and the eyes removed and dissected. The apoptotic markers Bax and Bcl-2 were assessed by Western Blot analyses in retina lysates. Gene-pathway network analysis was carried out in order to identify which pathways are involved in AMD.

Results : Treatment with Aβ oligomers induced a strong increase of Bax protein level (about 4-fold; p<0.01) and a significant reduction of Bcl-2 protein level (about 2-fold; p<0.05). Co-injection of TGF-β1 triggered a significant reduction of Bax protein induced by Aβ oligomers. The Bcl-2 and the PI3K-Akt are the most connected nodes, for genes and pathways respectively, in the enriched gene-pathway network common to AMD and Alzheimer’s disease (AD).

Conclusions : These data indicate that ITV injection of Aβ1-42 oligomers in rat induces molecular changes associated with apoptotic neuronal death in retina consistent with a potential pathogenetic role of Aβ oligomers in AMD. Bioinformatics analysis confirms that apoptosis pathways are impaired in AMD. Further, these findings suggest that human recombinant TGF-β1 can prevent retinal damage elicited by Aβ oligomers.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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