Severe preeclampsia is characterized by increased placental expression of galectin-1

被引:69
|
作者
Than, Nandor Gabor [1 ]
Erez, Offer [1 ,2 ]
Wildman, Derek E. [1 ,2 ,3 ]
Tarca, Adi L. [1 ]
Edwin, Samuel S. [1 ]
Abbas, Asad [1 ]
Hotra, John [1 ]
Kusanovic, Juan Pedro [1 ,2 ]
Gotsch, Francesca [1 ]
Hassan, Sonia S. [1 ,2 ]
Espinoza, Jimmy [1 ,2 ]
Papp, Zoltan [4 ]
Romero, Roberto [1 ,3 ]
机构
[1] Wayne State Univ, Hutzel Womens Hosp, Perinatol Res Branch, NICHD NIH DHHS, Detroit, MI 48201 USA
[2] Wayne State Univ, Dept Obstet & Gynecol, Sch Med, Detroit, MI 48201 USA
[3] Wayne State Univ, Ctr Mol Med & Genet, Sch Med, Detroit, MI 48201 USA
[4] Semmelweis Univ, Dept Obstet & Gynecol 1, H-1085 Budapest, Hungary
来源
关键词
glycocode; inflammation; lectin; pregnancy; semi-allograft; tolerance; trophoblast;
D O I
10.1080/14767050802041961
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Objective. Galectin-1 is a major anti-inflammatory protein expressed by the placenta and immune cells that can bias the character of inflammatory responses toward the Th2 type. Galectin-1 is expressed in immune privileged sites, it can facilitate immune tolerance and tumor immune escape, and it has been successfully used for the suppression of experimental autoimmune diseases as well as graft-versus-host disease in murine models. We propose that an abnormal immune response in some pregnancy complications may be associated with changes in placental expression of galectin-1. To test this hypothesis, we studied placental galectin-1 mRNA and protein expression and localization in women with preeclampsia (PE) and in those who delivered a small-for-gestational age (SGA) neonate. Study design. This cross-sectional study included pregnant women matched for gestational age at delivery in the following groups: (1) severe PE (n = 10), (2) severe PE complicated with SGA (n = 10), (3) SGA without PE (n = 10), and (4) controls (n = 10). Galectin-1 mRNA and protein were localized in placentas by in situ hybridization and immunofluorescence microscopy. Galectin-1 mRNA expression was determined by quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR), and galectin-1 protein content by Western blot. Non-parametric statistics were used for analysis. Results. (1) In normal term placentas, galectin-1 mRNA or immunofluorescence signals were detected in the trophoblasts, villous stromal cells, Hofbauer cells, endothelial cells of the villous blood vessels, and the villous stroma. (2) Placental galectin-1 mRNA expression was significantly higher in severe PE (with or without SGA) than in controls (1.47-fold, p = 0.004; 1.44-fold, p = 0.003, respectively) and in SGA (1.68-fold, p = 0.001; 1.64-fold, p = 0.001, respectively). (3) Trophoblasts in placentas of patients with severe PE had the most intense galectin-1 immunostaining. Conclusions. (1) We report for the first time the placental expression and localization of galectin-1 mRNA and demonstrate that the protein is abundantly present in third trimester human placentas. (2) Placental galectin-1 expression is higher in severe PE than in normal pregnancy regardless of the presence of SGA. (3) However, it is not altered in SGA without PE. We propose that the increased placental expression of galectin-1 in patients with severe PE may represent a fetal response to an exaggerated systemic maternal inflammation; thus, galectin-1 may be implicated in maternal-fetal immune tolerance in humans.
引用
收藏
页码:429 / 442
页数:14
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