Influence of histone acetylation on the modification of cytoplasmic and nuclear proteins by ADP-ribosylation in response to free radicals
Influence of histone acetylation on the modification of cytoplasmic and nuclear proteins by ADP-ribosylation in response to free radicals
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DOI：
10.1016/s0304-4165(96)00085-2
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发表时间：
1997-03-15
影响因子：
3
通讯作者：
Feinendegen, LE
中科院分区：
文献类型：
--
作者：
Bohm, L;Schneeweiss, FA;Feinendegen, LE
在生长培养基中添加5 mM n-丁酸钠抑制组蛋白去乙酰化酶，使V79、HeLa、小鼠B16、小鼠Fib/T和人T1肾细胞的总细胞蛋白[P-32]NAD（+）利用率和adp -核糖基化（ADPR）增加1.2-2.3倍。当adp核糖基酶受到挑战时将细胞暴露于。OH自由基（25 μ M CuSO4 2.8 mM H2O2） ADPR在正常和丁酸化细胞中分别增加5.7 ~ 6.0倍和3.2 ~ 4.0倍。对EDTA和自由基清除剂的反应支持自由基发生器的运行。sds -凝胶放射自显像的密度分析显示，丁酸盐暴露增加T1细胞adpr修饰的基础因子为1.1-1.9。的加法。OH自由基使正常细胞组蛋白ADPR修饰增加4.4-8.7倍，丁酸暴露细胞组蛋白ADPR修饰增加3.2-6.7倍。丁酸盐暴露可提高碱基水平的adpr修饰，并诱导DNA损伤引发的后续adpr修饰。这一结果与adpr修饰和组蛋白乙酰化具有重叠功能的观点是一致的，并且可能在染色质中引起类似的结构变化。
Inhibition of histone deacetylase by addition of 5 mM n-sodium butyrate to the growth medium increases the utilization of [P-32]NAD(+) and ADP-ribosylation (ADPR) of total cellular proteins of V79, HeLa, mouse B16, mouse Fib/T and human T1 kidney cells by a factor of 1.2-2.3. When the ADP-ribosylase is challenged by exposing cells to damage by . OH radicals (25 mu M CuSO4 2.8 mM H2O2) ADPR increases by factors of 5.7-6.0 and 3.2-4.0 in normal and butyrated cells, respectively. Operation of the free radical generator is supported by the response to EDTA and radical scavengers. Densitometric analysis of autoradiographs from SDS-gels show that butyrate exposure increases basal ADPR-modification of histones from T1 cells by factors of 1.1-1.9. Addition of . OH radicals increases the ADPR modifications of histones 4.4-8.7-fold in normal cells and 3.2-6.7-fold in butyrate exposed cells. Butyrate exposure elevates base level ADPR-modification and seduces subsequent ADPR-modification initiated by DNA damage. The results are consistent with the view that ADPR-modification and histone acetylation have overlapping functions and probably induce similar structural changes in chromatin.