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Submitted on August 20, 2002
Accepted on December 16, 2002
1 Division of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115; Department of Obstetrics and Gynecology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115; Departments of Obstetrics and Gynecology, and Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO 63110; Department of Genetics, Harvard Medical School, Boston, MA 02115
* To whom correspondence should be addressed. E-mail: maas{at}rascal.med.harvard.edu.
Human infertility and recurrent pregnancy loss caused by implantation defects are poorly understood. Hoxa-10 deficient female mice have severe infertility and recurrent pregnancy loss due to defective uterine implantation. Gene expression profiling experiments reveal that Hoxa-10 is an important regulator of two critical events in implantation -stromal cell proliferation and local immunosuppression. At the time of implantation, Hoxa-10 mediates the progesterone stimulated proliferation of uterine stromal cells. Hoxa-10 mutants express a stromal cell proliferation defect that is accompanied by quantitative or spatial alterations in the expression of two cyclin dependent kinase inhibitor (CKI) genes, p57 and p15. Hoxa-10 deficiency also leads to a severe local immunological disturbance, characterized by a polyclonal proliferation of T cells, that occurs in place of the normal progesterone-mediated immunosuppression in the peri-implantation uterus.
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