PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “TROPHOBLAST”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed2005

Lymphokine-activated killer cells induced from decidual lymphocytes reduce the angiogenic activity of trophoblasts by enhancing the release of soluble fms-like tyrosine kinase-1 from trophoblasts: an implication for the pathophysiology of preeclampsia.

T helper (Th)1 cytokine-predominating status and compromised placental vasculature is thought to be central to the pathogenesis of preeclampsia. However, it remains to be clarified how these two phenomena relate to each other. We have reported that lymphokine-activated killer (LAK) cells induced from decidual mononuclear cells (DMCs) with interleukin (IL)-2 expressed in preeclamptic placenta reduced the angiogenic activity of cytotrophoblasts (CTs). The objective of this study was to examine how LAK cells reduced the angiogenic activity of CTs. We investigated the angiogenesis-related molecules released from cultured CTs obtained from first trimester placenta that had been pretreated with either non-activated DMCs or LAK cells from DMCs. The amounts of vascular endothelial growth factor (VEGF), placenta growth factor (PlGF) and their antagonist, soluble fms-like tyrosine-kinase-1 (sFlt-1) released in CT culture media were measured using ELISA. CTs pretreated with LAK cells released more sFlt-1 compared with those pretreated with non-activated lymphocytes, and CTs pretreated with non-activated lymphocytes released more sFlt-1 compared with those without pretreatment. The release of total VEGF and free PlGF from CTs was not altered by pretreatment with DMCs. Thus, in preeclamptic placenta, LAK cells induced from DMCs by co-existing IL-2 may react to the invading CTs and enhance the release of sFlt-1 from CTs without any change of VEGF or PlGF secretion. This might result in the reduction of actual angiogenic potential of the VEGF system in decidua and the placental vascular system might be compromised, which may lead to the development of preeclampsia.

Cells, Cultured↗
PubMed1996

Osteogenic protein-1 is produced by human fetal trophoblasts in vivo and regulates the synthesis of chorionic gonadotropin and progesterone by trophoblasts in vitro.

Osteogenic protein-1 (OP-1/BMP-7), a member of the transforming growth factor (TGF-beta) superfamily of proteins, is shown to be expressed at sites of epithelial-mesenchymal tissue interaction during human fetal development. In the present study, we examined the expression of OP-1 in human placentas (5-11 weeks of gestation and full term) using in situ hybridization and immunohistochemistry methods. The results show that OP-1 was expressed in cytotrophoblasts (Langhans layer) of the chorionic villi in early and full term placentas. Employing highly purified cytotrophoblast cultures which fused to form functional syncytiotrophoblasts, we showed that exogenously added recombinant OP-1, in the presence of low serum concentration, reduced the secretion of chorionic gonadotropin and progesterone by 60% and 36%, respectively, compared with control cultures. The results suggest that osteogenic protein-1 is synthesized locally by cytotrophoblasts and may be involved in the regulation of human pregnancy by controlling reproductive hormonal secretion.

Animals↗