Expression of extracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase in the invasive trophoblasts at the human placental bed

被引:21
|
作者
Moon, K. C. [2 ]
Park, J. S. [1 ]
Norwitz, E. R. [3 ]
Kim, D. I. [2 ]
Oh, K. J. [1 ]
Park, C. -W. [1 ]
Jun, J. K. [1 ]
Syn, H. C. [1 ]
机构
[1] Seoul Natl Univ, Coll Med, Dept Obstet & Gynecol, Seoul 110744, South Korea
[2] Seoul Natl Univ, Coll Med, Dept Pathol, Seoul 110744, South Korea
[3] Yale Univ, Sch Med, Dept Obstet Gynecol & Reprod Sci, New Haven, CT USA
基金
新加坡国家研究基金会;
关键词
ERK; 1/2; p38 MAP kinase; trophoblast; preeclampsia; placental bed;
D O I
10.1016/j.placenta.2008.02.001
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Background: Mitogen- activated protein kinases (MAP kinases) participate in signal transduction pathways that control embryogenesis, cell differentiation, cell proliferation and cell death. The roles of extracellular signal-regulated kinase 1/2 (ERK 1/2) and p38 MAP kinase in the differentiation and invasion of human trophoblasts have been studied. However, the in vivo expression and activation of ERK 1/2 and p38 at the placental bed have not been elucidated. Methods: The study group consisted of placental bed biopsy tissues obtained from the pregnancies without preeclampsia (n = 24) and with preeclampsia (n = 8) between 31 and 40 weeks of gestation. We evaluated the expressions and phosphorylations of ERK 1/2 and p38 MAP kinase in the invasive trophoblasts in the placental bed tissues using immunohistochemistry. Results: p38 and phospho-p38 MAP kinase were not detected in invasive trophoblasts in cases or controls. ERK 1/2 and phospho-ERK 1/2 were positive in invasive trophoblasts albeit with variable staining. Phosphorylation of ERK 1/2 was significantly less frequent in invasive trophoblasts in placental bed biopsies from women with preeclampsia compared with normotensive controls. Conclusion: These findings suggest that preeclampsia is associated with decreased activation of ERK 1/2 in invasive trophoblasts in vivo. (C) 2008 Elsevier Ltd. All rights reserved.
引用
收藏
页码:391 / 395
页数:5
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