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/HIP2蛋白。由于单核细胞缺氧可上调LIG/HIP2蛋白的表达，而缺氧对单核细胞死亡的影响很小，因此LIG/HIP2可能对缺氧诱导的单核细胞死亡具有保护作用。LIG/HIP2蛋白及其与泛素系统其他组分的关联尚未完全确定。在本研究中，我们研究了以下内容：1)LIG/HIP2的蛋白谱和功能特性；2)LIG/HIP2在动脉粥样硬化组织巨噬细胞中的表达；3)缺氧对THP-1细胞源性巨噬细胞多泛素化和细胞死亡的影响。缺氧对巨噬细胞LIG/HIP2蛋白表达无影响。巨噬细胞中LIG/HIP2蛋白水平高于单核细胞。缺氧抑制巨噬细胞多泛素化，提高细胞内HIF-1α水平和细胞死亡。

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.