Differential expression of nestin in normal and pre-eclamptic human placentas

被引:11
作者
Hwang, Han-Sung
Cho, Nam-Hoon
Maeng, Yong-Sun
Kang, Myung-Hwa
Park, Yong-Won
Kim, Young-Han
机构
[1] Yonsei Univ, Coll Med, Dept Obstet & Gynecol, Seoul 120749, South Korea
[2] Yonsei Univ, Div Maternal Fetal Med, Seoul 120749, South Korea
[3] Yonsei Univ, Coll Med, Dept Diagnost Pathol, Seoul 120749, South Korea
[4] Yonsei Univ, Dept Biochem, Seoul 120749, South Korea
关键词
nestin; pre-eclampsia; placenta; endothelial cell;
D O I
10.1080/00016340701417018
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Background. Nestin is a type VI intermediate filament protein originally described in neural stem cells. Recent reports have documented nestin expression in endothelium of newly formed blood vessels and suggested its role as a marker of capacity for neovascularization and angiogenesis in endothelial cells. The aim of this study was to investigate the differential expression of nestin in normal and pre-eclamptic human placentas. Methods. Placental tissues from 12 women with severe pre-eclampsia and 15 gestational age-matched normotensive women were collected at the time of their cesarean section. Western blot analysis for each placental tissue was performed for nestin quantification. Immunohistochemical staining was employed to localize nestin-positive cells and to investigate differential staining intensity in each placental cell. Results. Nestin expression was detected in all of the normal and pre-eclamptic placental tissues by Western blotting. Compared with the normal placentas, tissues from severe pre-eclamptic placentas showed higher expression of nestin (p < 0.001). Nestin immunoreactivity was localized only to endothelial cells of chorionic villi. However, mesenchymal connective tissue cells, cytotrophoblasts, syncytiotrophoblasts, and decidual cells did not reveal any specific signal for nestin. Conclusions. We suggest that the capacity for neovascularization and angiogenesis in endothelial cell is increased in pre-eclamptic placenta compared to that from normal pregnancy. Such changes may be a compensatory mechanism for the reduced maternofetal exchanges and long-lasting fetal hypoxia in pre-eclamptic pregnancy. Furthermore, these changes in endothelial cells of chorionic villi in pre-eclamptic pregnancy may give an explanation for fetal response to pre-eclamptic conditions.
引用
收藏
页码:909 / 914
页数:6
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