Dataset Information

Endometriosis accelerates synchronization of early embryo cell divisions but does not change morphokinetic dynamics in endometriosis patients.

ABSTRACT:

Objective

The pathology of endometriosis and its impact on embryo development is still a black box in reproductive medicine. In this time-lapse study we investigated the influence of endometriosis on morphokinetic parameters of embryo development, taking variables of dynamic monitoring into account. Furthermore we evaluated reproductive medicine treatment outcome such as fetal heartbeat and live birth rate.

Methods

1148 embryos (control: n = 596, endometriosis: n = 552) were retrospectively analyzed. Patients were stimulated with GnRH antagonist protocol. After fertilization, embryos were incubated in a time-lapse system (EmbryoScope).

Results

The mixed-model analysis revealed a significant main effect of time (p<0.001), with post-hoc tests showing that any time needed to reach a specific developmental stage was significantly different from all the others (all p<0.001). Embryos of endometriosis patients showed the same absolute morphokinetic time parameters as the control group, however, synchronization of early embryo cell divisions (s2) was faster in endometriosis patients compared to the control group.

Conclusion

In general, endometriosis does not induce changes in early embryo morphokinetics. However, observed acceleration in cell cycle synchronization of embryo cleavage patterns might be a missing explanation for contradicting results in literature regarding the impairments in reproductive medicine treatment outcome of endometriosis patients.

SUBMITTER: Schenk M

PROVIDER: S-EPMC6675061 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Publications

Endometriosis accelerates synchronization of early embryo cell divisions but does not change morphokinetic dynamics in endometriosis patients.

Schenk Michael M Kröpfl Julia Maria JM Hörmann-Kröpfl Martina M Weiss Gregor G

PloS one 20190801 8

<h4>Objective</h4>The pathology of endometriosis and its impact on embryo development is still a black box in reproductive medicine. In this time-lapse study we investigated the influence of endometriosis on morphokinetic parameters of embryo development, taking variables of dynamic monitoring into account. Furthermore we evaluated reproductive medicine treatment outcome such as fetal heartbeat and live birth rate.<h4>Methods</h4>1148 embryos (control: n = 596, endometriosis: n = 552) were retro ...[more]

PMID: 31369616

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Project description:BackgroundA large body of research highlights the importance of early-life environmental impact on the health outcome in adulthood. However, whether early-life adversity (ELA) has any impact on the development of endometriosis is completely unclear. In this study, we tested the hypothesis that ELA, as manifested by neonatal separation, can accelerate the progression of endometriosis in mouse through activation of the adrenergic receptor ?2 (ADRB2) signaling pathway, leading to increased angiogenesis and progression of endometriotic lesions.MethodsEight female Balb/C mice, in late pregnancy, were used used for this study, which later gave birth to 22 female newborn pubs. Eleven additional female Balb/C mice were also used as donors of uterine tissues. The 22 newborn pubs were randomly divided into 2 equal-sized groups, maternal separation (MS) and no separation (NS). Pubs in the MS group were separated from their dams for 3?h/day from postnatal day (PND) 1 to 21, while those in the NS control remained in the home cage with their dams. In adulthood (8-week old), 3 mice in each group were randomly selected to undergo a battery of behavior tests. The remaining 8 mice in each group were induced with endometriosis by intraperitoneal injection of uterine fragments from donor mice. Four weeks after the induction, all mice were sacrificed and their endometriotic lesions were excised for quantification and then prepared for immunohistochemistry analysis.ResultsWe confirmed that MS during infancy resulted in anxiety and depression-like behaviors as previously reported. We also found that in MS mice the lesion weight was increased by over 2 folds and generalized hyperalgesia was also significantly increased as compared with NS mice. Immunostaining analysis demonstrated that MS accelerated the development of endometriosis likely through decreased dopamine receptor D2 (DRD2) expression and activation of the ADRB2/cAMP-response element binding protein (CREB) signaling pathway, leading to increased angiogenesis and progression of endometriotic lesions.ConclusionsExposure of female mouse pups to ELA such as MS during their infancy period accelerates the progression of endometriosis, possibly through altered neuronal wiring and hyperactivity of the hypothalamic-pituitary-adrenal axis.

Dataset Information

Endometriosis accelerates synchronization of early embryo cell divisions but does not change morphokinetic dynamics in endometriosis patients.

Objective

Methods

Results

Conclusion

Publications

Endometriosis accelerates synchronization of early embryo cell divisions but does not change morphokinetic dynamics in endometriosis patients.

Similar Datasets

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