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首页> 外文期刊>The FEBS journal >Altered expression of CD1d molecules and lipid accumulation in the human hepatoma cell line HepG2 after iron loading.
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Altered expression of CD1d molecules and lipid accumulation in the human hepatoma cell line HepG2 after iron loading.

机译：铁加载后，人肝癌细胞系HepG2中CD1d分子的表达改变和脂质蓄积。

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Iron overload in the liver may occur in clinical conditions such as hemochromatosis and nonalcoholic steatohepatitis, and may lead to the deterioration of the normal liver architecture by mechanisms not well understood. Although a relationship between the expression of ICAM-1, and classical major histocompatibility complex (MHC) class I molecules, and iron overload has been reported, no relationship has been identified between iron overload and the expression of unconventional MHC class I molecules. Herein, we report that parameters of iron metabolism were regulated in a coordinated-fashion in a human hepatoma cell line (HepG2 cells) after iron loading, leading to increased cellular oxidative stress and growth retardation. Iron loading of HepG2 cells resulted in increased expression of Nor3.2-reactive CD1d molecules at the plasma membrane. Expression of classical MHC class I and II molecules, ICAM-1 and the epithelial CD8 ligand, gp180 was not significantly affected by iron. Considering that intracellular lipids regulate expression of CD1d at the cell surface, we examined parameters of lipid metabolism in iron-loaded HepG2 cells. Interestingly, increased expression of CD1d molecules by iron-loaded HepG2 cells was associated with increased phosphatidylserine expression in the outer leaflet of the plasma membrane and the presence of many intracellular lipid droplets. These data describe a new relationship between iron loading, lipid accumulation and altered expression of CD1d, an unconventional MHC class I molecule reported to monitor intracellular and plasma membrane lipid metabolism, in the human hepatoma cell line HepG2.
机译：肝脏中的铁超载可能会出现在诸如血色病和非酒精性脂肪性肝炎等临床情况中，并且可能由于尚未充分了解的机制导致正常肝脏结构的恶化。尽管已经报道了ICAM-1，经典的主要组织相容性复合物（MHC）I类分子的表达与铁超负荷之间的关系，但尚未发现铁超负荷与非常规的MHC I类分子的表达之间的关系。在本文中，我们报道了铁负载后铁代谢的参数以协调的方式在人类肝癌细胞系（HepG2细胞）中得到调节，从而导致细胞氧化应激增加和生长迟缓。铁负载的HepG2细胞导致Nor3.2反应性CD1d分子在质膜上的表达增加。经典的MHC I和II类分子，ICAM-1和上皮CD8配体gp180的表达不受铁的显着影响。考虑到细胞内脂质调节细胞表面CD1d的表达，我们检查了铁载HepG2细胞中脂质代谢的参数。有趣的是，铁负载的HepG2细胞CD1d分子表达的增加与质膜外小叶中磷脂酰丝氨酸的表达增加以及许多细胞内脂质小滴的存在有关。这些数据描述了人类肝癌细胞系HepG2中铁负载，脂质蓄积和CD1d（一种非常规的MHC I类分子）表达变化之间的新关系，CD1d是非常规的MHC I类分子，用于监测细胞内和质膜脂质代谢。

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