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Hum. Reprod. Advance Access published online on October 3, 2008
Human Reproduction, doi:10.1093/humrep/den348
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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

Uterine natural killer cells and angiogenesis in recurrent reproductive failure

Siobhan Quenby1,3, Helena Nik1, Barbara Innes2, Gendie Lash2, Mark Turner1, Jo Drury1 and Judith Bulmer2

1 School of Reproductive and Developmental Medicine, University of Liverpool, First Floor, Liverpool Women’s Hospital, Crown Street, Liverpool L8 7SS, UK 2 Uterine Cell Signalling Group, Institute of Cellular Medicine, Newcastle University, Framlington Place, Newcastle upon Tyne NE2 4HH, UK

3 Correspondence address. E-mail:squenby{at}liv.ac.uk

BACKGROUND: Increased numbers of phenotypically unusual CD56bright CD16– uterine natural killer (uNK) cells have been associated with recurrent reproductive failure. uNK cells produce angiogenic growth factors and are potential regulators of decidual angiogenesis in early pregnancy. The final common mechanism for early pregnancy loss is thought to be early onset of the maternal circulation and excessive placental oxidative stress. We tested the hypothesis that increased uNK cells in preimplantation endometrium are associated with altered angiogenesis.

METHODS: Women with recurrent reproductive failure (n = 122) were investigated with uterine artery Doppler and endometrial biopsy. Immunohistochemistry was used to identify uNK, endothelial and vascular smooth muscle cells and image analysis was used to assess location, density and differentiation.

RESULTS: uNK cell density was positively correlated with the formation of blood (P = 0.005, r = 0.5) and lymphatic vessels (P = 0.0001, r = 0.6), spiral arteriole smooth muscle differentiation (P = 0.01, r = 0.5) and endometrial oedema (P = 0.004). The functional effect of this was a reduced uterine artery resistance to blood flow.

CONCLUSIONS: These data suggest that uNK cells may regulate angiogenesis in non-pregnant endometrium. The mechanisms of reproductive failure associated with increased uNK cell density appear to be increased angiogenesis and peri-implantation blood flow, which may lead to early maternal circulation and hence pregnancy failure due to excessive oxidative stress.

Key words: recurrent miscarriage/uNK cells/angiogenesis/recurrent implantation failure/endometrium

Submitted on April 15, 2008; resubmitted on July 22, 2008; accepted on August 29, 2008.


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