Hormones And Cytokines Which Increase The Synthesis Of Prostaglandin E2 In Syncytiotrophoblast Cells

Hormones And Cytokines Which Increase The Synthesis Of Prostaglandin E2 In  Syncytiotrophoblast Cells


Activators which stimulate cells by means of cell surface receptors also cause release of
prostaglandins from these cell membranes.  This mechanism of prostaglandin stimulation is
illustrated in Figure 2 from Dinarello’s paper Biology of Interleukin-1 (1).  Examples of this
mechanism include Interleukin-1 which induces a five-fold increase in Prostaglandin E2
production, a response that was density, time and dose dependent.  8-10 week human placentas
used (2).  hCG itself has also been shown to stimulate PGE2 synthesis in 9-12 week placentas at
physiological conditions.  The rate of PGE2 synthesis increased with a longer incubation period,
particularly in placentas of younger gestation.  Significant stimulation of PGE2 synthesis occurred
at 104 iu/1 hCG and continued to increase in a dose-dependent manner up to 5 x 106 iu/1 as seen in
9-10 week placental organ cultures.  There was considerable variation of PG production between
placentas of the same gestation (3).
 
Prostaglandin E2 is also synthesised in early pregnancy by macrophages and monocytes present in
the decidua (4) and at the materno-fetal interface (5) and by decidual stroma cells (6).  There is
therefore, clearly evidence of the presence of prostaglandin synthesis and stimulation of
Prostaglandin E2 production in the various cells of the materno-fetal interface in early pregnancy.
 
This study investigated the regulation of cyclo-oxygenase-2 (COX-2) gene by human CG (hCG) in
mucosal cells from fallopian tubes.  Culturing mucosal cells with increasing concentrations of hCG
also resulted in a dose-dependent increase in media PGE2 levels suggesting that the COX-2 protein
increased by hCG is catalytically active.  Although hCG treatment had no effect on the
transcription rate of COX-2 gene, it significantly increased the stability of COX-2 transcripts from
3.7h in the control to 7.3h after treatment.  (7)
 
GSH (reduced glutathione) stimulates prostaglandin synthesis but the presence of both L-
Epinephrine (catecholomine) and GSH are needed to achieve maximum conversion of arachidonic
acid into prostaglandins E2 in human term placentae. (8)
 

REFERENCES

1. DINARELLO C A.

 Biology of Interleukin-1.

 FASEB J. 1988;2:108-115.

 

2. SHIMONOVITZ S, YAGEL S, ANTEBY E, FINCI-YEHESKEL Z, ADASHI E Y, MAYER M, HURWITZ A.

Interleukin-1 stimulates Prostaglandin E2 production by human trophoblast cells from first and third trimesters.

 J. Clin Endocrinol Metab. 1995;80:1641-1646.

 

3. NORTH R A, WHITEHEAD R, LARKINS R G.

Stimulation by human chorionic gonadotrophin of prostaglandin synthesis by early human placental tissue.

 J. Clin Endocrinol Metab. 1991;73:60-70.

 

4. CORCORAN M L, KIBBY M C, KLEINMAN H K, WAHL L M.

Laminin sikvav peptide induction of monocyte/macrophage Prostaglandin E2

and matrix metalloproteinases.

 J. Biol Chem. 1995;270(8):10365-10368.

 

5. YAGEL S, PALTI Z, GALLILY R.

Prostaglandin E2 mediated suppression of human allo-reactivity by

first trimester fetal macrophages.

 Obstet Gynaecol. 1988;72(4):648-653.

 

6. PARHAR R S, KENNEDY T G, LALA P K.

 Suppression of leukocyte allo-reactivity by early gestational decidua.

 1. Characterisation of suppressor cells and suppressor molecules.

 Cell Immunol. 1988;116:392-400.

 

7. HAN S W, LEI Z M, RAO CH V.

Up-regulation of cyclo-oxygenase-2 gene suppression by chorionic

gonadotrophin in mucosal cells from human fallopian tubes.

 Edocrinol. 1996;137(7):2929-2937.

 

8.DUCHESME M J, THALER DAO H, CRASTES de PAULET A


 Prostaglandin syntheses in Human Placenta and Fetal Membranes


 Prostaglandins 1978;15(1):19-42
 

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