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Hum. Reprod. Advance Access published online on December 20, 2008
Human Reproduction, doi:10.1093/humrep/den461
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© The Author 2008. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Stress affects uterine receptivity through an ovarian-independent pathway

Eiji Kondoh1,2,{dagger}, Takako Okamoto1,{dagger}, Toshihiro Higuchi1, Keiji Tatsumi1,4, Tsukasa Baba1, Susan K. Murphy2, Kenji Takakura1, Ikuo Konishi1 and Shingo Fujii3

1 Department of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho Sakyo-ku, Kyoto 606-8507, Japan 2 Department of Obstetrics and Gynecology, Duke University Medical Center, Durham, NC 27708, USA 3 National Hospital Kyoto Medical Center, 1-1 Fukakusa Mukaihata-cho Fushimi-ku, Kyoto 612-8555, Japan

4 Correspondence address. Tel: +81-75-751-3269; Fax: +81-75-761-3967; E-mail: ktat{at}kuhp.kyoto-u.ac.jp

BACKGROUND: Although stress is known to disturb natural fertility through the inhibition of the hypothalamic–pituitary–gonadal (HPG) axis, the impact of stress on infertile women who receive exogenous gonadal hormones is not well defined. This is probably due to lack of experimental models for evaluating the impacts of stress through an ovarian-independent pathway. The objective of this study was to investigate the possible impact of stress on uterine receptivity, independent of HPG axis dysfunction, using a mouse implantation model maintained with hormone supplementation.

METHODS: Blastocysts from donor mice were transferred into the uterine lumen of ovariectomized (OVX) Balb/c female recipient mice following supplementation with estradiol and progesterone. The recipients were divided into two groups: those exposed (stress group) or not exposed (control group) to intermittent sonic exposure prior to embryo transfer (ET). The number of implantation sites (IS) was compared between these groups. Microarray analysis was performed to elucidate stress-induced molecular alterations in uteri during the implantation period. Sequential gene expression of leukemia inhibitory factor (Lif), an estradiol-inducible gene, was also analyzed using real-time PCR.

RESULTS: A non-mating OVX model with satisfactory implantation rates was established. The number of IS in the stress group (n = 20) was significantly less than that in the control group (n = 18) (Mann–Whitney test, P = 0.0375). Implantation-related genes and ovarian-hormone-responsive genes were repressed in the stress group despite ovarian hormone supplementation. The expression of Lif was suppressed in the stress group.

CONCLUSIONS: Stress can cause decreased uterine receptivity through an ovarian-independent pathway.

Key words: stress/fertility/uterine receptivity/Lif/gene expression

{dagger} These authors contributed equally to this work.

Submitted on August 22, 2008; resubmitted on October 13, 2008; accepted on November 11, 2008.


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