trichostatin-a and aluminum-tetrasulfophthalocyanine

Epigenetic processes are involved in regulation of cell functions and survival, but their role in responses of neurons and glial cells to oxidative injury is insufficiently explored. Here, we studied the role of DNA methylation and histone deacetylation in reactions of neurons and surrounding glial cells to photodynamic treatment that induces oxidative stress and cell death. Isolated crayfish stretch receptor consisting of a single mechanoreceptor neuron surrounded by glial cells was photosensitized with aluminum phthalocyanine Photosens that induced neuron inactivation, necrosis of the neuron and glia, and glial apoptosis. Inhibitors of DNA methylation 5-azacytidine and 5-aza-2'-deoxycytidine (decitabine) reduced the level of PDT-induced necrosis of glial cells but not neurons by 1.3 and 2.0 times, respectively, and did not significantly influence apoptosis of glial cells. Histone deacetylase inhibitors valproic acid and trichostatin A inhibited PDT-induced both necrosis and apoptosis of satellite glial cells but not neurons by 1.6-2.7 times. Thus, in the crayfish stretch receptor DNA methylation and histone deacetylation are involved in epigenetic control of glial but not neuronal necrosis. Histone deacetylation also participates in glial apoptosis.

Topics: Action Potentials; Animals; Apoptosis; Astacoidea; Azacitidine; Decitabine; DNA Methylation; Enzyme Inhibitors; Epigenesis, Genetic; Histone Deacetylase Inhibitors; Hydroxamic Acids; In Vitro Techniques; Indoles; Lasers; Mechanoreceptors; Necrosis; Neuroglia; Organometallic Compounds; Photic Stimulation; Photosensitizing Agents; Valproic Acid