Insufficient peroxiredoxin‐2 expression in uterine NK cells obtained from a murine model of abortion
Insufficient peroxiredoxin‐2 expression in uterine NK cells obtained from a murine model of abortion
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DOI：
10.1002/jcb.22893
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发表时间：
2011-03
影响因子：
4
通讯作者：
Guangjie Yin;Cui Li;B. Shan;Wenjing Wang;Hong Chen;Yanmin Zhong;J. Di;Qide Lin;Yi Lin
中科院分区：
文献类型：
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作者：
Guangjie Yin;Cui Li;B. Shan;Wenjing Wang;Hong Chen;Yanmin Zhong;J. Di;Qide Lin;Yi Lin
CBA/J × DBA/2 小鼠交配组合容易发生自发胚胎丢失，而 MHC 相同的 CBA/J × BALB/c 小鼠交配组合却能成功怀孕。这些观察结果的潜在机制尚不清楚。本研究采用多视觉免疫组织化学染色（IHC）、流式细胞术和蛋白质印迹分析检测CBA/J × DBA/2和CBA/J × BALB/c小鼠子宫自然杀伤（uNK）细胞中过氧化还原蛋白-2（PRX-2）的表达。在 IHC 分析中，证实了 PRX-2 和来自 Dolichos biflorus 凝集素（DBA-凝集素）的凝集素（DBA-凝集素）的共定位，并且 CBA/J × DBA/2 中 PRX-2+DBA-凝集素+细胞的频率显着低于 CBA/J × BALB/c。在流式细胞术和蛋白质印迹中，发现 CBA/J × DBA/2 小鼠中 PRX-2 的表达水平显着较低。使用中和抗体抑制 PRX-2 显着降低 CBA/J × DBA/2J 小鼠中 PRX-2 的表达，增加 uNK 细胞的细胞毒性，并增加胚胎损失的百分比。我们的数据表明，PRX-2 可能参与母胎耐受性的调节，并且该蛋白表达不足可能与 CBA/J × DBA/2J 小鼠胚胎损失增加相关。 J.细胞。生物化学。 112：773–781，2011。© 2010 Wiley-Liss, Inc.
The CBA/J × DBA/2 mouse mating combination is prone to spontaneous embryo loss, in contrast to the MHC‐identical CBA/J × BALB/c mating combination, which yields successful pregnancies. The underlying mechanisms for these observations are unclear. In this study, multi‐vision immunohistochemical staining (IHC), flow cytometry and Western blot analysis were used to detect peroxiredoxin‐2 (PRX‐2) expression in the uterine natural killer (uNK) cells from CBA/J × DBA/2 and CBA/J × BALB/c mice. In IHC analysis, co‐localization of PRX‐2 and lectin from Dolichos biflorus agglutinin (DBA‐lectin) was confirmed and the frequency of PRX‐2+DBA‐lectin+ cells was significantly lower in CBA/J × DBA/2 than CBA/J × BALB/c. In flow cytometry and Western blotting, PRX‐2 was found expressed at a significantly lower level in CBA/J × DBA/2 mice. PRX‐2 inhibition with a neutralizing antibody significantly decreased PRX‐2 expression, increased the cytotoxicity of uNK cells, and increased the percentage of embryo loss in CBA/J × DBA/2J mice. Our data suggest that PRX‐2 may be involved in the modulation of maternal–fetal tolerance and that insufficient expression of this protein may correlate with increased embryo loss in CBA/J × DBA/2J mice. J. Cell. Biochem. 112: 773–781, 2011. © 2010 Wiley‐Liss, Inc.