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首页> 外文期刊>Journal of Cellular Physiology >Activation of survival and apoptotic signaling pathways in lymphocytes exposed to palmitic acid.
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Activation of survival and apoptotic signaling pathways in lymphocytes exposed to palmitic acid.

机译：生存和凋亡信号激活通路在淋巴细胞暴露于棕榈酸。

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摘要

The toxicity of palmitic acid (PA) towards a human T-lymphocyte cell line (Jurkat) has been previously investigated but the mechanism(s) of PA action were unknown. In the current study, Jurkat cells were treated with sub-lethal concentrations of PA (50-150microM) and the activity of various signaling proteins was investigated. PA-induced apoptosis and mitochondrial dysfunction in a dose-dependent manner as evaluated by DNA fragmentation assay and depolarization of the mitochondrial membrane, respectively. PA treatment provoked release of cytochrome c from the inner mitochondrial membrane to the cytosol, activated members of the MAPK protein family JNK, p38, ERK, activated caspases 3/9, and increased oxidative/nitrosative stress. Exposure of cells to PA for 12 h increased insulin receptor (IR) and GLUT-4 levels in the plasma membrane. Insulin treatment (10 mU/ml/30 min) increased the phosphorylation of the IR beta-subunit and Akt. A correlation was found between DNA fragmentation and expression levels of both IR and GLUT-4. Similar results were obtained for PA-treated lymphocytes from healthy human donors and from mesenteric lymph nodes of 48-h starved rats. PA stimulated glucose uptake by Jurkat cells (in the absence of insulin), stimulated accumulation of neutral lipids (triglyceride), and other lipid classes (phospholipids and cholesterol ester) but reduced glucose oxidation. Our results suggest that parameters of insulin signaling and non-oxidative glucose metabolism are stimulated as part of a coordinated response to prompt survival in lymphocytes exposed to PA but at higher concentrations, apoptosis prevails. These findings may explain aspects of lymphocyte dysfunction associated with diabetes.
机译：棕榈酸的毒性对人类(PA)早期细胞系(Jurkat)以前调查的机制(s)PA行动是未知的。Jurkat细胞治疗剂量浓度的PA (50 - 150 microm)和各种信号蛋白的活性调查。线粒体功能障碍存在剂量依赖的相关性方式评价DNA碎片试验和线粒体膜的去极化,分别。从内部的线粒体细胞色素c胞质膜,激活的成员p38 MAPK蛋白质家族物,ERK激活还存在3/9,增加氧化/ nitrosative压力。增加胰岛素受体(IR)和GLUT-4水平在质膜。μ/毫升/ 30分钟)的磷酸化作用增加红外beta-subunit和Akt。发现DNA碎片和表达红外和GLUT-4水平。均获得PA-treated淋巴细胞人类健康的捐赠者和肠系膜淋巴结节点的48小时饥饿的老鼠。由Jurkat细胞吸收(没有胰岛素),刺激积累中立脂肪(甘油三酯)和其他脂类(磷脂和胆固醇酯),但降低了葡萄糖氧化。胰岛素信号和non-oxidative的参数葡萄糖代谢受到刺激的一部分协调一致的反应,以促使生存淋巴细胞暴露于PA但更高的浓度,细胞凋亡。淋巴细胞的发现可能解释方面功能障碍与糖尿病有关。

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