The Presence Of Prostaglandin E2 In The Early Syncytiotrophoblast Cells

The Presence Of Prostaglandin E2 In The Early Syncytiotrophoblast Cells


As we have found a relationship between hCG and pregnancy sickness between weeks 7 and 17
from LMP and a relationship between hCG and PGE2 synthesis in early trophoblast cells, it seems
reasonable to make further investigation of the possible association between Prostaglandin E2
levels and pregnancy sickness.
 
Kelly et al wrote, a mechanism by which the trophoblast could control its immediate environment in
the decidua and maternal blood may be through the release of prostaglandins (PG’s) and cytokines.  
This possibility has been investigated by measuring PG and several cytokines released from first
trimester trophoblastic villi cultured for 24 hours.  PGE is the main primary prostaglandin with a
release of 240 # 95 pg/mg/24 hours (1).  Because PGE can influence the function of many leukocytes
(particularly macrophages) by raising intracellular c’AMP concentrations, the release of hormonal
factors from the villous trophoblast might be important in pregnancy maintenance.  Trophoblastic
villi were obtained from women undergoing a first trimester 7-11 week termination of pregnancy (1).  
Johnson et al found the PGE2 was produced by a syncytial (differentiated) trophoblast.  Cells grown
beyond 24 hours in fibrin showed sustained expression of cyclo-oxygenase and this enzyme protein
expression correlated with increased PGE2 production in differentiated (syncytial) trophoblast.  Term
placentas were used (2).  Cheng et al found there was clear distinction in the distribution of
immunoreactive PGE2 among the different cell types of trophoblastic villi at 56 days of amenorrhoea
or less.  The cytoplasm of syncytiotrophoblast cells stained positively for PGE2, whereas, there was
very little, if any, staining in the cytotrophoblastic layer (3). At this stage of pregnancy prostaglandin
dehydrogenase (PGDH) was present in abundance in cytotrophoblast cells of chorionic villi but is
virtually absent from syncytiotrophoblast. This PGDH in cytotrophoblast cells would prevent access
to prostaglandin E2 (PGE2) generated in the syncytiotrophoblast to the fetal blood vessels (4).
The syncytiotrophoblast is devoid of Prostaglandin dehydrogenase (PGDH) and, therefore,
contains high levels of PGE2.  This distribution of catabolising enzyme leaving some
unmetabolised PGE2 only on the maternal aspect of syncytiotrophoblast cells might be important
where these villi, and particularly the syncytiotrophoblast cells are in direct contact with maternal
blood (3).
Infusion of PGE2 into the maternal circulation of an in vitro dual perfused human placental
cotyledon preparation did not result in increased PGE2 efflux but PGEM (metabolite of PGE2) was
increased demonstrating a rapid efficient metabolism by the placenta. There was no significant
transfer of PGE2 across to the fetal circulation, although there was some transfer but in the form of
inactivated PGEM. There was no significant interconversion of PGE2 to PGF2H$by the 9-keto-
reducase pathway (5). 

REFERENCES



1. KELLY R W, CARR G G, ELLIOTT C L, TULPPALA H, CRITCHLEY H O D.

 Prostaglandin and cytokine release by trophoblastic villi.

 Human Reprod. 1995;10(12):3289-3292.


2. JOHNSON R D, WALSH S W, EVERSON W V, NELSON D M.

 Differentiation and growth on a fibrin matrix modulate the cyclo-oxygenase expression and thromboxane production by cultured human placental trophoblasts.

 Prostaglandins, Leukotrienes and essential fatty acids. 1995;52:21-27.

3. CHENG L, KELLY R W, THONG K J, HUME R, BAIRD D T.

 The effect of mifepristone (RU 486) on the immunohistochemical distribution of Prostaglandin E and its metabolite in decidual and chorionic tissue in early pregnancy.

 J. Clin Endocrinol Metab. 1993;77:873-877.

 

4. CHENG L, KELLY R W, THONG K J, HUME R, BAIRD D T.

The effects of mifepristone (RU 486) on prostaglandin dehydrogenase in decidual and chorionic tissue in early pregnancy.

 Human Reprod. 1993;8:705-709.

 

5. GREYSTOKE A P, KELLY R W, BENEDIKTSSON R, RILEY S C.

Transfer and metabolism of Prostaglandin E2 in the dual perfused human placenta.

Placenta 2000;21(1):109-114.

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