Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inhibitors of histone deacetylases are frequently used against ischemia-induced injury, but the specific mechanisms of their action are poorly understood. Here, we report that following a 5-7-h oxygen-glucose deprivation (OGD) acetylation of histone H4 at residue K16 (H4K16Ac) decreases by 40-80% in both PC12 cells and primary neurons. This effect can be reverted by treatment with trichostatin A, or by supplementation with acetyl-CoA. A decrease in H4K16Ac levels can affect the expression of mitochondrial uncoupling protein 2 (UCP2), huntingtin-interacting protein 1 (HIP1) and Notch-pathway genes in a cell-specific manner. Thus, H4K16 acetylation is important for responses to ischemia and cell energy stress, and depends on both cytosolic and mitochondrial acetyl-CoA.
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PMID:In vitro ischemia decreases histone H4K16 acetylation in neural cells. 2547 88