Histone 3 (k14) acetilation in hyperbilirubinmia. Histone 3 (k14) acetilation in hyperbilirubinmia

Bilirubin toxicity to the CNS has been widely studied for decades, and shown impacting potential toxic/adaptation mechanisms by a significant modulation of gene expression, suggesting that mechanisms having crucial role on the regulation of gene expression, such as epigenetic mechanisms, should have a strong impact in unconjugated bilirubin toxicity. In this work, we followed the levels of histone 3 acetylation (H3K14Ac) in the cerebellum (Cll) of the developing (2, 9, 17 days after the birth and in adult age) Gunn rat (the natural model for neonatal hyperbilirubinemia and kernicterus) by Western blot, discovering an age specific alteration of the H3K14Ac in the hyperbilirubinemic animals. Then, the H3K14Ac linked chromatin was immune-precipitated and submitted to sequencing (ChIP-Seq). The GeneOntology analysis revealed that almost the 45% of H3K14Ac ChiP-Seq TSS-promoter genes were involved in the CNS development. Overall design: ChIP-Seq of the H3K14ac chomatin in hyperbilirubinmic (jj) and cotrols cerebella from P9 Gunn rats. 4 jj (2 runs) and 3 ctrl (1 run) were used.