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Mol. Hum. Reprod. Advance Access published online on September 30, 2008
Molecular Human Reproduction, doi:10.1093/molehr/gan055
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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

Calpain5 expression is regulated by HOXA10 in human endometrial cells and aberrantly regulated in endometriosis

Ivan Penna1,2, Hongling Du1, Rui Ferriani2 and Hugh S. Taylor1

1Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT, USA 2Department of Obstetrics and Gynecology of Ribeirão Preto Medical School/ São Paulo University, Ribeirão Preto, SP, Brazil

Correspondence: Hugh S Taylor, MD Division of Reproductive Endocrinology and Infertility Yale University School of Medicine 333 Cedar Street New Haven, Connecticut 06520 hugh.haylor{at}yale.edu Phone 203-785-4005 Fax 203-785-7819

Calpains have been implicated in the regulation of apoptosis. Here we identified Calpain5 as a target of HOXA10 transcriptional regulation in endometrial cells as well as its aberrant regulation in endometriosis. Histologically confirmed biopsies of endometriosis were obtained from twenty women. Eutopic endometrium was collected by endometrial biopsy from thirty controls and from the twenty subjects with endometriosis. First trimester decidual samples were obtained from five subjects at the time of pregnancy termination. Immunohistochemistry (IHC) was used to identify Calpain5 expression. Calpain5 was expressed in endometrial stromal and glandular cells throughout the menstrual cycle and in decidua. Calpain5 protein expression was decreased in both stromal and glandular cells from women with endometriosis compared to that of fertile controls. Human endometrial stromal and epithelial cell lines were transfected with pcDNA/HOXA10, HOXA10 siRNA or respective controls. qRT-PCR was performed to determine expression of HOXA10 and Calpain5 in each group. Transfection of HESC cells with a HOXA10 expression construct led to increased Calpain5 expression, while transfection with siRNA resulted in decreased expression. In conclusion, calpain5 expression is regulated by HOXA10. Calpain5 expression was decreased in endometriosis likely as a result of decreased HOXA10 expression. Decreased apoptosis in endometrial cells may promote the development of endometriosis through a pathway involving HOXA10, Calpain5 and Caspase.

Key Words: Calpain5/HOXA10/endometrium/endometriosis/apoptosis

Supported by NIH HD36887, NIH U54 HD052668, CAPES/Br

Submitted on April 7, 2008; resubmitted on September 16, 2008; accepted on September 19, 2008.


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