Saturated Fatty Acid-induced cytotoxicity in liver cells does not involve phosphatase and tensin homologue deleted on chromosome 10.
Saturated Fatty Acid-induced cytotoxicity in liver cells does not involve phosphatase and tensin homologue deleted on chromosome 10.
复制标题
饱和脂肪酸诱导的肝细胞细胞毒性不涉及 10 号染色体上磷酸酶和张力蛋白同源物的缺失。
DOI：
10.1155/2013/514206
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发表时间：
2013
影响因子：
2.2
通讯作者：
Pagliassotti,MichaelJ
中科院分区：
文献类型：
--
作者：
Wang,Dong;Wei,Yuren;Frye,Melinda;Gentile,ChristopherL;Pagliassotti,MichaelJ
肝脏特异性缺失10号染色体上的肿瘤抑制磷酸酶和张力蛋白同源物（PTEN）可诱导脂肪变性和对胰岛素的超敏反应。诱导内质网应激和细胞死亡的饱和脂肪酸似乎增加PTEN，而不诱导内质网应激或细胞死亡的不饱和脂肪酸减少这种蛋白质。在本研究中，在H4IIE和HepG2肝细胞中检查了PTEN在饱和脂肪酸诱导的细胞毒性中的作用。棕榈酸盐和硬脂酸盐增加了PTEN的表达，而不饱和脂肪酸，油酸盐和亚油酸盐，在两种细胞类型中减少了PTEN的表达。siRNA介导的PTEN敲低不会增加肝细胞甘油三酯储存或减少棕榈酸或硬脂酸介导的ER应激或凋亡。这些结果表明，在这些肝细胞模型中和不存在胰岛素的情况下，PTEN在饱和脂肪酸诱导的细胞毒性中不起显著作用。
Liver specific deletion of the tumor suppressor phosphatase and tensin homologue deleted on chromosome 10 (PTEN) induces steatosis and hypersensitivity to insulin. Saturated fatty acids, which induce endoplasmic reticulum stress and cell death, appear to increase PTEN, whereas unsaturated fatty acids which do not induce endoplasmic reticulum stress or cell death reduce this protein. In the present study, the role of PTEN in saturated fatty acid‐induced cytotoxicity was examined in H4IIE and HepG2 liver cells. Palmitate and stearate increased the expression of PTEN, whereas the unsaturated fatty acids, oleate and linoleate, reduced PTEN expression in both cell types. SiRNA‐mediated knockdown of PTEN did not increase liver cell triglyceride stores or reduce palmitate‐ or stearate‐mediated ER stress or apoptosis. These results suggest that PTEN does not play a significant role in saturated fatty acid‐induced cytotoxicity in these liver cell models and in the absence of insulin.