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Primary Rod and Cone Degeneration Is Prevented by HDAC Inhibition

Dragana Trifunović1, Eleni Petridou2, Antonella Comitato3

  • 1Institute for Ophthalmic Research, University of Tuebingen, Tuebingen, Germany. dragana.trifunovic@uni-tuebingen.de.

Advances in Experimental Medicine and Biology
|May 4, 2018
PubMed

Insights

Histone deacetylase (HDAC) over-activation drives photoreceptor cell death in inherited retinal diseases. Inhibiting HDAC with drugs like trichostatin A and vorinostat shows promise for protecting rod and cone cells, potentially preserving vision.

Area of Science:

  • Ophthalmology
  • Neuroscience
  • Genetics

Background:

  • Inherited retinal degeneration involves photoreceptor cell death.
  • Over-activation of histone deacetylases (HDAC) is a common feature in both rod and cone photoreceptor degeneration.
  • Specific mouse models, rd10 for rod degeneration and cpfl1 for cone degeneration, exhibit excessive HDAC activity.

Purpose of the Study:

  • To evaluate the potential of pharmacological HDAC inhibition for preventing photoreceptor degeneration.
  • To assess the efficacy of HDAC inhibitors in models of primary rod and cone degeneration.

Main Methods:

  • In vivo treatment of cpfl1 mice with trichostatin A (TSA).
  • Treatment of rd10 retinal explant cultures with vorinostat (SAHA).
  • Assessment of photoreceptor survival and protection following HDAC inhibition.

Main Results:

  • A single in vivo TSA treatment significantly protected cone photoreceptors in cpfl1 mice.
  • HDAC inhibition with vorinostat significantly improved rod photoreceptor survival in rd10 retinal explant cultures.
  • Pharmacological HDAC inhibition demonstrates neuroprotective effects in models of retinal degeneration.

Conclusions:

  • Targeted neuroprotection via HDAC inhibition is feasible in vivo.
  • HDAC inhibitors offer a potential therapeutic strategy for preserving vision in patients with rod and cone dystrophies.
  • These findings provide hope for maintaining vision in inherited retinal degeneration patients.
Keywords:
Cone degenerationHDACInhibitionNeuroprotectionRod degenerationTrichostatin A (TSA)Vorinostat (SAHA)cpfl1rd10

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