Acute Strenuous Exercise Induces an Imbalance on Histone H4 Acetylation/Histone Deacetylase 2 and Increases the Proinflammatory Profile of PBMC of Obese Individuals

Acute Strenuous Exercise Induces an Imbalance on Histone H4 Acetylation/Histone Deacetylase 2 and Increases the Proinflammatory Profile of PBMC of Obese Individuals
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DOI:
10.1155/2017/1530230
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发表时间:
2017-01-01
影响因子:
--
通讯作者:
Romao, Pedro R. T.
Romao, Pedro R. T.
中科院分区:
生物学2区
文献类型:
--
作者:
Dorneles, Gilson P.;Boeira, Maria Carolina R.;Romao, Pedro R. T.

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本研究评估了整体组蛋白H4乙酰化(H4 ac),组蛋白去乙酰化酶2(HDAC 2)活性,以及促炎细胞因子和单核细胞表型的瘦和肥胖男性运动后的反应。10名瘦和10名肥胖的久坐不动的人提交了一个会议的剧烈运动,外周血单个核细胞(PBMC)在体外刺激脂多糖(LPS)。分析了总体H4 ac水平、PBMC中的HDAC 2活性以及IL-6、IL-8和TNF-α产生。根据CD 14和CD 16的表达确定单核细胞表型。在静息状态下,肥胖个体的促炎性CD 14(+)CD 16(+)单核细胞频率较高。脂多糖诱导的全球H4 ac和IL-6,IL-8和TNF-α的生产显着增加,主要是在肥胖个体。运动后,两组IL-8、TNF-α水平及外周血CD 14(+)、CD 16(+)频率均明显升高。此外,运动还诱导了组蛋白H4的显着的高乙酰化和降低HDAC 2活性在两个非刺激和LPS刺激的PBMC的肥胖个体。我们的数据表明,肥胖影响H4 ac水平,剧烈运动通过H4 ac/HDAC 2的不平衡导致肥胖中慢性低度炎症特征增强。
This study evaluated the response of global histone H4 acetylation (H4ac), histone deacetylase 2 (HDAC2) activity, as well as the production of proinflammatory cytokines and monocyte phenotypes of lean and obese males after exercise. Ten lean and ten obese sedentary men were submitted to one session of strenuous exercise, and peripheral blood mononuclear cells (PBMC) were stimulated in vitro with lipopolysaccharide (LPS). Global H4ac levels, HDAC2 activity in PBMC, and IL-6, IL-8, and TNF-alpha production were analyzed. Monocyte phenotype was determined in accordance with the expression of CD14 and CD16. At rest, obese individuals presented higher frequency of proinflammatory CD14(+) CD16(+) monocytes. LPS induced a significant augment in global H4ac and in the production of IL-6, IL-8, and TNF-alpha mainly in obese individuals. After exercise, the increased production of IL-8 and TNF-alpha and peripheral frequency of CD14(+) CD16(+) were observed in both groups. In addition, exercise also induced a significant hyperacetylation of histone H4 and decreased HDAC2 activity in both nonstimulated and LPS-stimulated PBMC of obese individuals. Our data indicate that the obesity impacts on H4ac levels and that strenuous exercise leads to an enhanced chronic low-grade inflammation profile in obesity via an imbalance on H4ac/HDAC2.