Inhibin and Activin Production in Human Placenta

Qu, Jianping; Thomas, Karl

doi:10.1210/edrv-16-4-485

Cited by 89 publications

(13 citation statements)

References 268 publications

(318 reference statements)

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“…BMP-7/ osteogenic protein-1 is expressed by cytotrophoblast cells rather than by the ST, but appears to play a negative paracrine role in steroidogenesis (Martinovic et al 1996). In contrast to its low expression in the uterus, inhibin A is abundantly produced by the placenta (Qu & Thomas 1995). This is predominantly due to syncytial expression, and its co-expression with beta-glycan (Jones et al 2002b, Ciarmela et al 2003) is consistent with inhibin acting as a functional antagonist for activin in the placenta.…”

Section: Regulation Of Trophoblast Invasionmentioning

confidence: 99%

TGF-β superfamily expression and actions in the endometrium and placenta

et al. 2006

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Transforming growth factor b (TGFb) superfamily members are closely associated with tissue remodelling events and reproductive processes. This review summarises the current state of knowledge regarding the expression and actions of TGFb superfamily members in the uterus, during the menstrual cycle and establishment of pregnancy. TGFbs and activin b subunits are abundantly expressed in the endometrium, where roles in preparation events for implantation have been delineated, particularly in promoting decidualisation of endometrial stroma. These growth factors are also expressed by epithelial glands and secreted into uterine fluid, where interactions with preimplantation embryos are anticipated. Knockout models and embryo culture experiments implicate activins, TGFbs, nodal and bone morphogenetic proteins (BMPs) in promoting pre-and post-implantation embryo development. TGFb superfamily members may therefore be important in the maternal support of embryo development. Following implantation, invasion of the decidua by fetal trophoblasts is tightly modulated. Activin promotes, whilst TGFb and macrophage inhibitory cytokine-1 (MIC-1) inhibit, trophoblast migration in vitro, suggesting the relative balance of TGFb superfamily members participate in modulating the extent of decidual invasion. Activins and TGFbs have similar opposing actions in regulating placental hormone production. Inhibins and activins are produced by the placenta throughout pregnancy, and have explored as a potential markers in maternal serum for pregnancy and placental pathologies, including miscarriage, Down's syndrome and pre-eclampsia. Finally, additional roles in immunomodulation at the materno-fetal interface, and in endometrial inflammatory events associated with menstruation and repair, are discussed.

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Section: Regulation Of Trophoblast Invasionmentioning

confidence: 99%

TGF-β superfamily expression and actions in the endometrium and placenta

et al. 2006

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“…Therefore, the absence of an activin ,BC subunit signal in the RNAase protection for the TGCTs led us to conclude that activin PC is not expressed in substantial amounts in these tumours. The combined expression of inhibin a-and jB subunit expression in one non-seminoma may be the result of extra-embryonal differentiation, because expression of these subunits has been described in trophoblastic cells and fetal membranes (Qu and Thomas, 1995). Apparently, this is not a general phenomenon as the other mature teratoma/yolk sac tumour in our panel did not give rise to relatively high expression levels for inhibin a-and fiB subunits; in addition, pure yolk sac or mature teratoma tumours were negative for inhibin a-subunit mRNA.…”

Section: Inhibin Subunits and Follistatinmentioning

confidence: 99%

Human testicular germ cell tumours express inhibin subunits, activin receptors and follistatin mRNAs

Schaik

Wierikx²,

Looijenga³

et al. 1997

Br J Cancer

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Summary Germ cell development is influenced by activin and inhibin, which are produced by Sertoli cells. Activin also affects differentiation of mouse embryonal carcinoma cells, which, to a certain extent, resemble the embryonal carcinoma component of germ cell tumours. Therefore, the expression of inhibin/activin subunits, of activin receptors and of the activin-binding protein follistatin was studied in testicular germ cell tumours, using RNAase protection assays. Testicular germ cell tumours of adolescents and adults (TGCTs) and spermatocytic seminomas expressed activin type and type 11 receptors (ActRi and ActRII respectively). Seminomas expressed significantly lower levels of ActRIIA (P<0.05, Mann-Whitney U-test) and higher levels of ActRIA (P<0.05) and ActRIB (P<0.05) compared with non-seminomas. All tumours expressed inhibin n-subunit transcripts, which are a prerequisite for activin synthesis. Non-seminomas contained significantly higher levels of the inhibin PA subunit (P<0.001) compared with seminomas. No activin PC subunit transcripts could be demonstrated by RNAase protection. Inhibin a-subunit expression was absent in the spermatocytic seminomas, in six out of nine seminomas and in 10 out of 11 nonseminomas. Follistatin was expressed predominantly in non-seminomas and spermatocytic seminomas. This expression of activin type and type 11 receptors in combination with expression of inhibin 5-subunits indicates that activin may act as a para-or autocrine factor in the regulation of growth and differentiation of tumours of human germ cells.

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“…In pregnancy, the placenta is the major source of activin in the maternal circulation (de Kretser et al 1994, Qu & Thomas 1995, Wallace & Healy 1996, Fowler et al 1998, secreting predominantly activin A (Fowler et al 1998). Maternal serum levels of activin A increase from about mid-pregnancy to a peak close to term (Muttukrishna et al 1996, Fowler et al 1998, Schneider-Kolsky et al 2002, falling quickly after birth (Fowler et al 1998).…”

Section: Introductionmentioning

confidence: 99%

Oxidative stress increases placental and endothelial cell activin A secretion

Mandang

Manuelpillai

Wallace

2007

Journal of Endocrinology

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Circulating levels of activin A are significantly increased in women with preeclampsia when compared with those with a normal pregnancy. The mechanisms underlying these increased levels are unknown. We undertook these studies to explore whether oxidative stress might be the mechanism. We exposed trophoblast explants, human umbilical vein endothelial cells (HUVECs) and peripheral blood monocytes to oxidative stress in vitro using xanthine/xanthine oxidase (X/XO), measuring activin A and isoprostane in conditioned media and mRNA for activin b A in explants and HUVECs. We also measured isoprostane and activin A in serum from 21 women with preeclampsia and from 20 women with a normal pregnancy. Treatment with X/XO significantly increased 8-isoprostane production from placental explants, HUVECs and monocytes, indicative of oxidative stress, and significantly increased activin A output from placental explants (139 . 1G27 . 4 per mg wet weight vs 322 . 9G 89 . 7 pg/ml per mg wet weight, PZ0 . 02) and from HUVECs (1 . 2G0 . 2 vs 3 . 2G1 . 8 ng/ml, PZ0 . 04). There was no effect on activin A output from monocytes. X/XO significantly increased b A mRNA in placental explants but not in HUVECs. Maternal plasma levels of 8-isoprostane and activin A were significantly higher in women with preeclampsia when compared with controls (333 . 8G70 vs 176 . 3G 26 . 2 pg/ml, PZ0 . 04 and 49 . 5G7 vs 13 . 1G1 . 2 ng/ml, P!0 . 001 respectively). In the women with preeclampsia, but not in those with a normal pregnancy, circulating levels of 8-isoprostane and activin A were significantly and positively correlated (r 2 Z0 . 72; P!0 . 001). These data suggest that oxidative stress may be one of the mechanisms underlying increased circulating activin A in preeclampsia.

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Inhibin and Activin Production in Human Placenta

Cited by 89 publications

References 268 publications

TGF-β superfamily expression and actions in the endometrium and placenta

TGF-β superfamily expression and actions in the endometrium and placenta

Human testicular germ cell tumours express inhibin subunits, activin receptors and follistatin mRNAs

Oxidative stress increases placental and endothelial cell activin A secretion

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