The Acetylation of Histone H3 at Lys24 is Accompanied by Delayed Expression of Neuroprotective Proteins Bcl-2 and BDNF in the Neocortex of Rats Exposed to Severe Hypoxia: the Effect of Postconditioning

Recent studies imply that epigenetic mechanisms may play a key role in the pathogenesis of severe neurological diseases. We have previously shown that acetylation of histone H3 at Lys 24 (H3acK24) is involved in the formation of acute adaptive response of the brain to hypoxia. Here, using an immunohistochemical technique, we compared the effects of severe hypoxia and severe hypoxia followed by neuroprotective postconditioning using mild hypoxia on the expression of the antiapoptotic Bcl-2 protein, neurotrophin BDNF, and the level of H3acK24 in the neocortex of rats in delayed period (4 days). The delayed upregulation of Bcl-2, BDNF, and H3acK24 was observed in the sensorimotor cortex of rats subjected to severe hypoxia, suggesting late induction of the pro-adaptive neuronal processes. Postconditioning by three episodes of mild hypoxia returned the levels of H3acK24 to the control level and partially abolished the upregulation of Bcl-2 and BDNF. The findings demonstrate an important role of H3 acetylation at Lys24 in the regulation of apoptosis and neuroplasticity in response to hypoxia.