The Pro-Inflammatory Role of Adiponectin at the Maternal-Fetal Interface

被引:17
|
作者
McDonald, Emily A. [1 ]
Wolfe, Michael W. [1 ]
机构
[1] Univ Kansas, Med Ctr, Dept Mol & Integrat Physiol, Inst Reprod Hlth & Regenerat Med, Kansas City, KS 66160 USA
关键词
Adiponectin; immune response; placenta; HIGH-MOLECULAR-WEIGHT; VASCULAR ENDOTHELIAL-CELLS; FACTOR-KAPPA-B; GLOBULAR ADIPONECTIN; INSULIN-RESISTANCE; TROPHOBLAST CELLS; GENE-EXPRESSION; ADIPOSE-TISSUE; PROTEIN ACRP30; PREECLAMPSIA;
D O I
10.1111/j.1600-0897.2010.00971.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Problem A successful pregnancy is contingent on maternal tolerance of the immunologically foreign fetus. Prevalent diseases such as preeclampsia arise in part due to an inappropriate immune response by the placenta. A number of molecules have been proposed to temper cellular response to pro-inflammatory mediators, including CD24 and Siglec10. Methods Cytotrophoblast cells from healthy term placentas were treated with adiponectin in vitro and analyzed with qPCR and ELISA-based assays. Immunohistochemistry was performed on term villous sections and cultured trophoblasts. Results Treatment with adiponectin increased expression of IL-1 beta and IL-8. Term villi express CD24 in cytotrophoblasts and the syncytiotrophoblast, and Siglec10 by the syncytiotrophoblast. Treatment of trophoblast cells with adiponectin increased Siglec10 expression. Conclusion These data describe a role for adiponectin in enhancing pro-inflammatory signals in in vitro syncytialized trophoblasts. Additionally, this represents the first time the CD24/Siglec10 pathway has been implicated in a trophoblast response to a pro-inflammatory mediator.
引用
收藏
页码:128 / 136
页数:9
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