Allograft inflammatory factor-1 augments macrophage phagocytotic activity and accelerates the progression of atherosclerosis in ApoE-/- mice.
Allograft inflammatory factor-1 augments macrophage phagocytotic activity and accelerates the progression of atherosclerosis in ApoE-/- mice.
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DOI：
10.3892/ijmm.21.2.181
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发表时间：
2008-02
影响因子：
5.4
通讯作者：
T. Mishima;K. Iwabuchi;S. Fujii;Shinya Tanaka;H. Ogura;Keiko Watano-Miyata;Naoki Ishimori;Y. Andoh;Y. Nakai;C. Iwabuchi;M. Ato;A. Kitabatake;H. Tsutsui;K. Onoé
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文献类型：
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作者：
T. Mishima;K. Iwabuchi;S. Fujii;Shinya Tanaka;H. Ogura;Keiko Watano-Miyata;Naoki Ishimori;Y. Andoh;Y. Nakai;C. Iwabuchi;M. Ato;A. Kitabatake;H. Tsutsui;K. Onoé
同种异体移植炎性因子（AIF）-1，最初从慢性排斥反应的大鼠心脏移植物中克隆，在包括动脉粥样硬化在内的各种炎症条件下被诱导。我们使用小鼠AIF-1转染巨噬细胞和AIF-1转基因（AIF-1 Tg）小鼠，分析AIF-1过表达对巨噬细胞吞噬功能和动脉粥样硬化发展的影响。AIF-1转染子对乳胶珠和大肠杆菌的吞噬作用显著增强。coli BioParticles以及与载体对照相比乙酰化低密度脂蛋白（LDL）的掺入。用来自AIF-1 Tg小鼠的引发的腹膜渗出液细胞获得一致的结果。当AIF-1 Tg小鼠与载脂蛋白E敲除小鼠（ApoE-/-）杂交时，这些AIF-1 Tg ApoE-/-小鼠与ApoE-/-小鼠相比发生了显著增加的动脉粥样硬化病变。这些结果表明，增强AIF-1的表达，导致增加纳入变性LDL的巨噬细胞和促进动脉粥样硬化血管病变的发展。
Allograft inflammatory factor (AIF)-1, originally cloned from a rat heart allograft under chronic rejection, is induced in various inflammatory conditions including atherosclerosis. Using mouse AIF-1 transfected macrophages and AIF-1 transgenic (AIF-1 Tg) mice, we analyzed the influence of AIF-1 overexpression on macrophage phagocytosis and the development of atherosclerosis. The AIF-1 transfectants showed significantly increased phagocytosis of latex beads and E. coli BioParticles as well as incorporation of acetylated low-density lipoprotein (LDL) compared to those of vector controls. Concordant results were obtained with elicited peritoneal exudate cells from AIF-1 Tg mice. When AIF-1 Tg mice were crossbred with apolipoprotein E knockout mice (ApoE-/-), these AIF-1 Tg ApoE-/- mice developed significantly increased atherosclerotic lesions compared to ApoE-/- mice. These results suggest that enhanced AIF-1 expression leads to augmented incorporation of degenerated LDL by macrophages and promotes development of atherosclerotic vasculopathy.