Protection of retinal cells from ischemia by a novel gap junction inhibitor

Satyabrata Das, Dingbo Lin, Snehalata Jena, Aibin Shi, Srinivas Battina, Duy H. Hua, Rachel Allbaugh, Dolores J. Takemoto

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


Retinal cells which become ischemic will pass apoptotic signal to adjacent cells, resulting in the spread of damage. This occurs through open gap junctions. A class of novel drugs, based on primaquine (PQ), was tested for binding to connexin 43 using simulated docking studies. A novel drug has been synthesized and tested for inhibition of gap junction activity using R28 neuro-retinal cells in culture. Four drugs were initially compared to mefloquine, a known gap junction inhibitor. The drug with optimal inhibitory activity, PQ1, was tested for inhibition and was found to inhibit dye transfer by 70% at 10 μM. Retinal ischemia was produced in R28 cells using cobalt chloride as a chemical agent. This resulted in activation of caspase-3 which was prevented by PQ1, the gap junction inhibitor. Results demonstrate that novel gap junction inhibitors may provide a means to prevent retinal damage during ischemia.

Original languageEnglish (US)
Pages (from-to)504-508
Number of pages5
JournalBiochemical and Biophysical Research Communications
Issue number4
StatePublished - Sep 5 2008

Bibliographical note

Funding Information:
We gratefully acknowledge the kind gift of R28 cells from Dr. Gail Seigel. This work was supported by EYRO113421 to D.J.T., NIH R01AG025500, NSF CHE-0555341 and American Heart Association 0750115Z to D.H.H.


  • Caspase-3
  • Cobalt Chloride (CoCl)
  • Gap junctions
  • HIF1α
  • Hypoxia
  • Ischemia
  • PQ1
  • Retinal degeneration


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