Müller glia activation by VEGF-antagonizing drugs: An in vitro study on rat primary retinal cultures

Lucia Gaddini, Monica Varano, Andrea Matteucci, Cinzia Mallozzi, Marika Villa, Flavia Pricci, Fiorella Malchiodi-Albedi

Research output: Contribution to journalArticlepeer-review


The effects of the anti-Vascular Endothelial Growth Factor (VEGF) drugs ranibizumab and aflibercept were studied in Müller glia in primary mixed cultures from rat neonatal retina. Treatment with both agents induced activation of Müller glia, demonstrated by increased levels of Glial Fibrillary Acidic Protein. In addition, phosphorylated Extracellular-Regulated Kinase 1/2 (ERK 1/2) showed enhanced immunoreactivity in activated Müller glia. Treatment with aflibercept induced an increase in K+ channel (Kir) 4.1 levels and both drugs upregulated Aquaporin 4 (AQP4) in activated Müller glia. The results show that VEGF-antagonizing drugs influence the homeostasis of Müller cells in primary retinal cultures, inducing an activated phenotype. Upregulation of Kir4.1 and AQP4 suggests that Müller glia activation following anti-VEGF drugs may not depict a detrimental gliotic reaction. Indeed, it could represent one of the mechanisms able to contribute to the therapeutic effects of these drugs, particularly in the presence of macular edema.

Original languageEnglish
Pages (from-to)158-163
Number of pages6
JournalExperimental Eye Research
Publication statusPublished - Apr 1 2016


  • Aflibercept
  • Aquaporin 4
  • Glial Fibrillary Acidic Protein
  • K channel 4.1
  • Müller glia
  • Primary retinal cultures
  • Ranibizumab
  • Vascular Endothelial Growth Factor

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience


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