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Volume 91, Issue 2, Pages 489-499 (February 2009)


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Infertile women with isolated polycystic ovaries are deficient in endometrial expression of osteopontin but not αvβ3 integrin during the implantation window

Renée DuQuesnay, MRCOGa, Corrina Wright, M.B., B.Ch.c, Anita Abdul Aziz, Ph.D.a, Gordon W.H. Stamp, FRCPath.c, Geoffrey H. Trew, MRCOGb, Raul A. Margara, M.D.b, John O. White, Ph.D.dCorresponding Author Informationemail address

Received 30 July 2006; received in revised form 19 November 2007; accepted 19 November 2007. published online 18 March 2008.

Objective

To characterize possible endometrial defects in infertile women with isolated PCO morphology.

Design

Prospective study.

Setting

An academic hospital with an IVF unit.

Patient(s)

Women with primary unexplained infertility and isolated PCO, fertile women, and women with infertility secondary to male factor.

Intervention(s)

Thirty-one women (fertile and with male factor infertility) had endometrial sampling across the menstrual cycle. Nine fertile women and 10 infertile women with isolated PCO had sampling on day LH +7, adjusted for histologic dating.

Main Outcome Measure(s)

Expression of αvβ3 and its ligand, osteopontin, were determined using real-time quantitative polymerase chain reaction and immunohistochemistry. In vitro regulation of osteopontin was assessed using the Ishikawa cell line.

Result(s)

Cyclic variations revealed a fall in integrin αvβ3 mRNA during the secretory phase with concomitant up-regulation of osteopontin mRNA. Immunohistochemistry on day LH +7 demonstrated a significant reduction in expression of osteopontin in the isolated PCO group with no difference in expression of αvβ3. In vitro studies confirmed up-regulation of osteopontin by estrogen with no apparent effect of androgen.

Conclusion(s)

These results demonstrate an apparent reduction of osteopontin expression, important in cell–cell adhesion, during the window of implantation in infertile women with isolated PCO morphology.

a Institute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Hospital, London W12 0NN, United Kingdom

b Division of Paediatrics, Obstetrics and Gynaecology, Imperial College London, Hammersmith Hospital, London W12 0NN, United Kingdom

c Department of Histopathology, Imperial College London, Hammersmith Hospital, London W12 0NN, United Kingdom

d Reproductive Biology Research Group, Institute of Life Science, Swansea University School of Medicine, Swansea, United Kingdom

Corresponding Author InformationReprint requests: John O. White, Ph.D., Reproductive Biology Research Group, Institute of Life Science, Swansea University School of Medicine, Swansea SA2 8PP, United Kingdom (FAX: 01792602280).

 R.D. has nothing to disclose. C.W. has nothing to disclose. A.A.A. has nothing to disclose. G.W.H.S. has nothing to disclose. G.H.T. has nothing to disclose. R.A.M. has nothing to disclose. J.O.W. has nothing to disclose.

 Supported by The Wellcome Trust, Grant Number 069773/Z/02/Z, and The Institute of Obstetrics and Gynaecology Trust Fund, Hammersmith Hospital.

PII: S0015-0282(07)04129-5

doi:10.1016/j.fertnstert.2007.11.063


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