Application of LIG gene to identify the early atherosclerotic lesions in human

在常氧和缺氧条件下，THP-1细胞来源的单核细胞和巨噬细胞表达LIG/HIP 2蛋白。由于LIG/HIP 2蛋白表达在单核细胞中被缺氧上调，并且缺氧对单核细胞的细胞死亡的影响很小，LIG/HIP 2可能对缺氧诱导的单核细胞细胞死亡具有保护作用。LIG/HIP 2蛋白质谱和蛋白质与泛素系统的其他组分的关联尚未完全确定。在这项研究中，我们研究了以下内容：1）LIG/HIP 2的蛋白质谱和功能特性，2）LIG/HIP 2在动脉粥样硬化组织巨噬细胞中的表达，以及3）缺氧对THP-1细胞衍生的巨噬细胞的多聚泛素化和细胞死亡的影响。低氧对巨噬细胞LIG/HIP 2蛋白表达无影响。巨噬细胞中LIG/HIP 2蛋白水平高于单核细胞。缺氧可抑制巨噬细胞多聚泛素化，增加细胞内HIF-1α水平，促进巨噬细胞死亡。

Under normoxic and hypoxic conditions, THP-1 cell-derived monocytes and macrophages express LIG/HIP2 proteins. Because the LIG/HIP2 protein expression was upregulated by hypoxia in monocytes, and there was minimal effect of hypoxia on the cell death of monocytes, LIG/HIP2 may have a protective role against the hypoxia-induced cell death of monocytes. The LIG/HIP2 protein profile and the association of the protein with the other components of the ubiquitin system have not been fully determined. In this study, we examined the following, 1), the protein profile and functional properties of LIG/HIP2, 2) the expression of LIG/HIP2 in the atherosclerotic tissue macrophages, and 3) the influence of hypoxia on poly-ubiquitination and cell death of THP-1 cell-derived macrophages. Hypoxia had no effect on LIG/HIP2 protein expression by macrophages. The LIG/HIP2 protein level in macrophages is higher than that in monocytes. Hypoxia suppressed the poly-ubiquitination and enhanced both the intracellular HIF-1α level and the cell death of macrophages.