September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Antiangiogenic Effect of a Novel Fusion Protein PFMC inhibiting NFKB pathway on Corneal Alkali Injury Rat Model
Author Affiliations & Notes
  • Juan Pablo Salica
    Ophthalmology, Universidad Austral, Pilar, Buenos Aires, Argentina
    Nanomedicine and Vision Group, Universidad Austral, ilarP, Argentina
  • Alejandro Fichetti
    Nanomedicine and Vision Group, Universidad Austral, ilarP, Argentina
  • Eduardo Chuluyan
    Pharmacology Department, Universidad de Buenos Aires, Capital Federal, Argentina
  • Diego Guerrieri
    Pharmacology Department, Universidad de Buenos Aires, Capital Federal, Argentina
  • Juan E Gallo
    Ophthalmology, Universidad Austral, Pilar, Buenos Aires, Argentina
    Nanomedicine and Vision Group, Universidad Austral, ilarP, Argentina
  • Footnotes
    Commercial Relationships   Juan Salica, None; Alejandro Fichetti, None; Eduardo Chuluyan, None; Diego Guerrieri, None; Juan Gallo, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 3514. doi:
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      Juan Pablo Salica, Alejandro Fichetti, Eduardo Chuluyan, Diego Guerrieri, Juan E Gallo; Antiangiogenic Effect of a Novel Fusion Protein PFMC inhibiting NFKB pathway on Corneal Alkali Injury Rat Model. Invest. Ophthalmol. Vis. Sci. 2016;57(12):3514.

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

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Abstract

Purpose : To investigate the effect of the Fusion Protein FPMC (SLPI and Cementoin) on the NFkB (nuclear factor kappa light chain enhancer of activated B cells) pathway during the acute inflammation process on a rat corneal alkali injury model.

Methods : An alkali injury was produced with a filter paper of 3 mm with 1 N NaOH during 40 seconds in the right cornea of 27 Sprague Dawley rats under isoflurane anesthesia. They were treated with 10 ul of FPMC (0,2 ug/ ul; n=9), SLPI (0,2 ug/ul; n=9) or vehicle (n=9) topically, four times a day. Three rats of each group were sacrificed at 6 hours, 4 days and 10 days after injury. Corneas were studied by slit lamp and pictured before euthanasia. Corneal Neovascularization (CNV) area was quantified. NFkB was assayed by Western Blot. Vascular endothelial growth factor (VEGF) protein was evaluated by immunohistochemistry. VEGF and NF-kB mRNA levels were determined by reverse transcription-polymerase chain reaction (RT-PCR).

Results : The alkali injury induced CNV area was reduced in PFMC treated group. The NFkB curve on the acute inflammation process was significantly reduced by FPMC in comparison to the SLPI and Buffer treatment. VEGF and NFkB mRNA levels were lower on the Fusion Protein treated group.

Conclusions : The fusion protein FPMC demonstrated to reduce corneal neovascularization. The inhibition of NFkB pathway is one of the proven mechanisms of action of this novel protein.

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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