Stroke is one of the leading reasons of human death. Ischemic penumbra that surrounds the stroke-induced infarction core is potentially salvageable, but molecular mechanisms of its formation are poorly known. Histone acetylation induces chromatin decondensation and stimulates gene expression. We studied the changes in the levels and localization of histone acetyltransferases HAT1 and PCAF in penumbra after photothrombotic stroke (PTS, a stroke model). In PTS, laser irradiation induces local occlusion of cerebral vessels after photosensitization by Rose Bengal. HAT1 and PCAF are poorly expressed in normal cortical neurons and astrocytes, but they are overexpressed 4–24 h after PTS. Their predominant localization in neuronal nuclei did not change after PTS, but their levels in the astrocyte nuclei significantly increased. Western blotting showed the increase of HAT1 and PCAF levels in the cytoplasmic fraction of the PTS-induced penumbra. In the nuclear fraction, PCAF level did not change, and HAT1 was overexpressed only at 24 h post-PTS. PTS-induced upregulation of HAT1 and PCAF in the penumbra was mainly associated with overexpression in the cytoplasm of neurons and especially astrocytes. HAT1 and PCAF did not co-localize with TUNEL-positive cells that indicated their nonparticipation in PTS-induced apoptosis.

中风是人类死亡的主要原因之一。可以挽救中风诱发的梗塞核心周围的缺血性半影​​，但其形成的分子机制尚不清楚。组蛋白乙酰化诱导染色质脱凝并刺激基因表达。我们研究了血栓性中风（PTS，中风模型）后半影中组蛋白乙酰转移酶HAT1和PCAF的水平和定位的变化。在PTS中，Rose Bengal进行光敏后，激光照射会引起脑血管的局部阻塞。HAT1和PCAF在正常的皮质神经元和星形胶质细胞中表达较差，但在PTS后4–24小时过表达。它们在PTS后在神经元核中的主要定位没有改变，但是它们在星形胶质细胞核中的水平显着增加。蛋白质印迹显示PTS诱导的半影的细胞质部分中的HAT1和PCAF水平增加。在核级分中，PCAF水平没有变化，HAT1仅在PTS后24小时过表达。PTS诱导的半影区HAT1和PCAF的上调主要与神经元特别是星形胶质细胞的细胞质中的过表达有关。HAT1和PCAF未与TUNEL阳性细胞共定位，这表明它们不参与PTS诱导的细胞凋亡。