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Oral Selumetinib Does Not Negatively Impact Photoreceptor Survival in Murine Experimental Retinal Detachment

Colleen M Cebulla1, Bongsu Kim1, Valerie George1

  • 1Havener Eye Institute, Department of Ophthalmology and Visual Science, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States.

Investigative Ophthalmology & Visual Science
|January 26, 2019
PubMed
Abstract

Insights

MEK inhibitors (MEKi) did not increase photoreceptor death in experimental retinal detachment (RD), despite blocking protective MAPK/ERK signaling. This suggests other pathways may compensate for MEKi effects during RD.

Area of Science:

  • Ophthalmology
  • Neuroscience
  • Oncology

Background:

  • Mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling offers neuroprotection in certain retinal damage models.
  • The role of MAPK/ERK signaling in neuronal survival during retinal detachment (RD) remains unclear.
  • Serous RDs are a common side effect of MEK inhibitors (MEKi), used in cancer therapy to block MAPK/ERK signaling.

Purpose of the Study:

  • To investigate the hypothesis that MEK inhibitor (MEKi) treatment exacerbates photoreceptor death in experimental retinal detachment (RD).

Main Methods:

  • Experimental retinal detachment (RD) was induced in C57BL/6 mice.
  • Mice received daily doses of the MEKi selumetinib.
  • Photoreceptor survival (TUNEL assay) and outer nuclear layer (ONL) thickness were analyzed.
  • Immunofluorescence was used to assess phospho-ERK1/2 (pERK), glial fibrillary acidic protein (GFAP), and Iba-1.

Main Results:

  • Selumetinib blocked pERK accumulation in Müller glia within detached retinas.
  • No increase in serous RDs, photoreceptor death, or ONL thinning was observed in selumetinib-treated mice compared to controls.
  • Selumetinib prevented the increase in intraretinal microglia/macrophage Iba-1 intensity and amoeboid morphology, while not altering retinal gliosis.

Conclusions:

  • In experimental RD, selumetinib blocked Müller glia pERK accumulation and modulated microglia/macrophage responses but did not impair photoreceptor survival.
  • These findings align with good visual acuity in patients experiencing transient RDs during MEK inhibitor therapy.
  • Potential compensation by alternative neuroprotective pathways in the retina may occur during MEK inhibition in RD.

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