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Insufficient peroxiredoxin‐2 expression in uterine NK cells obtained from a murine model of abortion
Author(s) -
Yin Guangjie,
Li Cui,
Shan Bin,
Wang Wenjing,
Chen Hong,
Zhong Yanmin,
Di Jingfang,
Lin Qide,
Lin Yi
Publication year - 2011
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.22893
Subject(s) - flow cytometry , biology , western blot , microbiology and biotechnology , immunohistochemistry , andrology , blot , lectin , embryo , decidua , immunology , fetus , medicine , placenta , pregnancy , biochemistry , gene , genetics
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.