Prednisolone Alters Endometrial Decidual Cells and Affects Decidual-Trophoblast Interactions

Grbac, Eliza; So, Teresa; Varshney, Swati; Williamson, Nicholas A.; Dimitriadis, Evdokia; Menkhorst, Ellen

doi:10.3389/fcell.2021.647496

Cited by 5 publications

(4 citation statements)

References 70 publications

(81 reference statements)

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“…In another study, a low concentration of LIF in uterine flushing fluid at day 26 was predictive of subsequent implantation and the LIF concentration was significantly lower in the pregnant group ( 75 ). Prednisolone treatment reduced the expression of human endometrial stromal fibroblasts (hESFs) cytokines (IL-6, IL-11, IL-18, LIF, and LIFR), however it had no effect on classic decidualization marker gene expression (prolactin or insulin like growth factor binding protein 1) or secretion by decidualized hESF ( 76 ).…”

Section: Discussionmentioning

confidence: 99%

Pro- and anti-inflammatory cytokines and growth factors in patients undergoing in vitro fertilization procedure treated with prednisone

Piekarska,

Dratwa,

Radwan

et al. 2023

Front. Immunol.

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Embryo implantation is a key moment in pregnancy. Abnormal production of pro- and anti-inflammatory cytokines, their receptors and other immune factors may result in embryo implantation failure and pregnancy loss. The aim of this study was to determine the profile of selected pro- and anti-inflammatory factors in the blood plasma of patients undergoing in vitro fertilization (IVF) and control women who achieved pregnancy after natural conception. The examined patients were administered steroid prednisone. We present results concern the plasma levels of IFN-ɣ, BDNF, LIF, VEGF-A, sTNFR1 and IL-10. We found that IVF patients receiving steroids differed significantly from patients who were not administered such treatment in terms of IFN-γ and IL-10 levels. Moreover, IVF patients differed in secretion of all tested factors with the fertile controls. Our results indicated that women who secrete at least 1409 pg/ml of sTNFR1 have a chance to become pregnant naturally and give birth to a child, while patients after IVF must achieve a concentration of 962.3 pg/ml sTNFR1 in blood plasma for successful pregnancy. In addition, IVF patients secreting VEGF-A above 43.28 pg/ml have a greater risk of miscarriage or a failed transfer in comparison to women secreting below this value. In conclusion, fertile women present a different profile of pro- and anti-inflammatory cytokines, and growth factors compared to patients with recurrent implantation failure (RIF).

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Section: Discussionmentioning

confidence: 99%

Pro- and anti-inflammatory cytokines and growth factors in patients undergoing in vitro fertilization procedure treated with prednisone

Piekarska,

Dratwa,

Radwan

et al. 2023

Front. Immunol.

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“…The trophoblast is therefore described as a "pseudo-malignant" tissue or a "physiological metastasis" (Ferretti et al, 2007). Abnormal EVT functions are linked to adverse pregnancy outcomes such as RSA and preeclampsia (Fisher, 2015;Grbac et al, 2021). However, the exact cause of the abnormal or shallow placentation associated with these adverse pregnancy outcomes remains uncertain.…”

Section: Discussionmentioning

confidence: 99%

DOCK1 insufficiency disrupts trophoblast function and pregnancy outcomes via DUSP4-ERK pathway

Xu,

Liu,

Zeng

et al. 2023

Life Sci. Alliance

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Abnormal trophoblast function is associated with diseases such as recurrent spontaneous abortion, pre-eclampsia, and preterm birth, and endangers maternal and fetal health. However, the underlying regulatory mechanisms remain unclear. In this study, we found DOCK1 expression is decreased in the placental villi of patients with recurrent spontaneous abortion, and that its expression determined the invasive properties of extravillous trophoblasts (EVTs), highlighting a previously unknown role of DOCK1 in regulating EVT function. Furthermore, DOCK1 deficiency disturbed the ubiquitinated degradation of DUSP4, leading to its accumulation. This caused inactivation of the ERK signaling pathway, resulting in inadequate EVT migration and invasion. DOCK1 was implicated in regulating the ubiquitin levels of DUSP4, possibly by modulating the E3 ligase enzyme HUWE1. The results of our in vivo experiments confirmed that the DOCK1 inhibitor TBOPP caused miscarriage in mice by inactivating the DUSP4/ERK pathway. Collectively, our results revealed the crucial role of DOCK1 in the regulation of EVT function via the DUSP4-ERK pathway and a basis for the development of novel treatments for adverse pregnancy outcomes caused by trophoblast dysfunction.

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“…PRL secretion by decidualized hESF (culture media collected on days 3 and 14) was quantified by ELISA as per the manufacturer’s instructions (DuoSet kit #DY682, R&D systems) ( 23 ).…”

Section: Methodsmentioning

confidence: 99%

Endometrial stromal cell miR-19b-3p release is reduced during decidualization implying a role in decidual-trophoblast cross-talk

Menkhorst

Rainczuk

et al. 2023

Front. Endocrinol.

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IntroductionA healthy pregnancy requires successful blastocyst implantation into an adequately prepared or ‘receptive’ endometrium. Decidualization of uterine endometrial stromal fibroblast cells (hESF) is critical for the establishment of a healthy pregnancy. microRNAs (miRs) are critical regulators of cellular function that can be released by a donor cell to influence the physiological state of recipient cells. We aimed to determine how decidualization affects hESF miR release and investigated the function of one decidualization regulated miR, miR-19b-3p, previously shown to be associated with recurrent pregnancy loss.MethodmiR release by hESF was determined by miR microarray on culture media from hESF decidualized in vitro for 3 and 14 days by treatment with oestradiol and medroxyprogesterone acetate. Cellular and whole endometrial/decidual tissue miR expression was quantified by qPCR and localized by in situ hybridization. The function of miR-19b-3p in HTR8/Svneo trophoblast cells was investigated using real time cell analysis (xCELLigence) and gene expression qPCR.ResultsFrom our miR screen we found that essentially all hESF miR release was reduced following in vitro decidualization, significantly so for miR-17-5p, miR-21-3p, miR-34c-3p, miR-106b-5p, miR-138-5p, miR-296-5p, miR-323a-3p, miR-342-3p, miR-491-5p, miR-503-5p and miR-542-5p. qPCR demonstrated that miR-19b-3p, 181a-2-3p and miR-409-5p likewise showed a significant reduction in culture media following decidualization but no change was found in cellular miR expression following decidualization. In situ hybridization localized miR-19b-3p to epithelial and stromal cells in the endometrium and qPCR identified that miR-19b-3p was significantly elevated in the cycling endometrium of patients with a history of early pregnancy loss compared to normally fertile controls. Functionally, overexpression of miR-19b-3p significantly reduced HTR8/Svneo trophoblast proliferation and increased HOXA9 expression.DiscussionOur data demonstrates that decidualization represses miR release by hESFs and overexpression of miR-19b-3p was found in endometrial tissue from patients with a history of early pregnancy loss. miR-19b-3p impaired HTR8/Svneo proliferation implying a role in trophoblast function. Overall we speculate that miR release by hESF may regulate other cell types within the decidua and that appropriate release of miRs by decidualized hESF is essential for healthy implantation and placentation.

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Prednisolone Alters Endometrial Decidual Cells and Affects Decidual-Trophoblast Interactions

Cited by 5 publications

References 70 publications

Pro- and anti-inflammatory cytokines and growth factors in patients undergoing in vitro fertilization procedure treated with prednisone

Pro- and anti-inflammatory cytokines and growth factors in patients undergoing in vitro fertilization procedure treated with prednisone

DOCK1 insufficiency disrupts trophoblast function and pregnancy outcomes via DUSP4-ERK pathway

Endometrial stromal cell miR-19b-3p release is reduced during decidualization implying a role in decidual-trophoblast cross-talk

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