Open AccessDifferential expression of nestin in normal and pre‐eclamptic human placentas
Author(s) -
HWANG HANSUNG,
CHO NAMHOON,
MAENG YONGSUN,
KANG MYUNGHWA,
PARK YONGWON,
KIM YOUNGHAN
Publication year - 2007
Publication title -
acta obstetricia et gynecologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.401
H-Index - 102
eISSN - 1600-0412
pISSN - 0001-6349
DOI - 10.1080/00016340701417018
Subject(s) - nestin , angiogenesis , decidua , syncytiotrophoblasts , neovascularization , biology , andrology , placenta , pathology , fetus , immunohistochemistry , medicine , stem cell , pregnancy , microbiology and biotechnology , neural stem cell , cancer research , genetics
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.