Peer-Reviewed Journal Details
Mandatory Fields
Ruslan I. Dmitriev, Dmitri B. Papkovsky
2015
January
Febs Letters
In vitro ischemia decreases histone H4K16 acetylation in neural cells
Published
Optional Fields
Histone (de)acetylation; H4K16; Histone acetyltransferase; Hypoxia; Ischemic tolerance; Oxygen and glucose deprivation
589
1
138
144
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.
http://www.sciencedirect.com/science/article/pii/S0014579314008540
10.1016/j.febslet.2014.11.038
Grant Details
Science Foundation Ireland