July 2019
Volume 60, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2019
Aflibercept and Ranibizumab modulate retinal pigmented epithelial cells viability/proliferation and protect them from oxidative stress by mechanisms related to their cross talk with vascular endothelial cells
Author Affiliations & Notes
  • Stefano De Cillà
    University Hospital Maggiore della Carità, Novara, Novara, Italy
    Health Sciences, University East Piedmont “A.Avogadro”, Novara, Italy
  • Caterina Toma
    University Hospital Maggiore della Carità, Novara, Novara, Italy
  • Stela Vujosevic
    University Hospital Maggiore della Carità, Novara, Novara, Italy
  • Andrea Muraca
    University Hospital Maggiore della Carità, Novara, Novara, Italy
  • Serena Farruggio
    Translational Medicine, University East Piedmont "A.Avogadro", Novara, Italy
  • Giulia Raina
    Translational Medicine, University East Piedmont "A.Avogadro", Novara, Italy
  • Elena Grossini
    Translational Medicine, University East Piedmont "A.Avogadro", Novara, Italy
  • Footnotes
    Commercial Relationships   Stefano De Cillà, None; Caterina Toma, None; Stela Vujosevic, None; Andrea Muraca, None; Serena Farruggio, None; Giulia Raina, None; Elena Grossini, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science July 2019, Vol.60, 5404. doi:
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      Stefano De Cillà, Caterina Toma, Stela Vujosevic, Andrea Muraca, Serena Farruggio, Giulia Raina, Elena Grossini; Aflibercept and Ranibizumab modulate retinal pigmented epithelial cells viability/proliferation and protect them from oxidative stress by mechanisms related to their cross talk with vascular endothelial cells. Invest. Ophthalmol. Vis. Sci. 2019;60(9):5404.

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

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Abstract

Purpose : To investigate how nitric oxide (NO) release and mitochondrial function contribute to the protective action of anti-VEGF (Ranibizumab and Aflibercept) on retinal pigmented epithelium (RPE), performing co-culture experiments between RPE and umbilical vascular endothelial cells (HUVEC)

Methods : Knowing that RPE and HUVEC cross-talk is of fundamental relevance for the maintenance of outer retina structure and function, co-cultures RPE/HUVEC were performed and exposed to Ranibizumab/Aflibercept in the absence or presence of NO synthase (NOS) inhibitor and phosphatidylinositol-3-kinase/protein kinase B (PKB), extracellular-signal-regulated kinases 1/2 (ERK1/2) and p38 mitogen activated protein kinase (p38 MAPK) blockers. Following intra and inter-cellular mechanisms were examined: NO release, cellular proliferation/migration, cell viability, mitochondrial membrane potential, apoptosis and PKB, p38 MAPK and ERK1/2 expression/activation. Specific kits were used for cell viability, NO and reactive oxygen species detection, apoptosis and mitochondrial membrane potential measurement. Western Blot was performed for detection of apoptotic markers and other kinases. Cell migration was measured by wound healing assay and cell proliferation using XCELLigence.

Results : In physiologic conditions, Aflibercept/Ranibizumab increased NO release in a dose and time-dependent way in RPE cells co-cultured with HUVEC. Opposite results were obtained in RPE cells pretreated with hydrogen peroxide. Both anti-VEGF prevented the fall of cell viability and of mitochondrial membrane potential and increased cell migration. Those actions were inhibited in presence of specific blockers. Aflibercept/Ranibizumab counteracted the changes of apoptotic markers, NOS, PKB and ERK1/2 caused by peroxidation.

Conclusions : In the present study, the potential role of NO and mitochondria in the protective action of Aflibercept/Ranibizumab on RPE was described. In particular, after stimulation with both anti-VEGF, HUVEC seem to release paracrine factors involved in RPE response to anti-VEGF.

This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.

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