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Division of Genetics (M.W.M.Y., S.E.C., A.F., Y.D., S.M., R.L.M.), Department of Medicine and Department of Obstetrics and Gynecology (M.W.M.Y., D.J.S.), Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115; Departments of Obstetrics and Gynecology, and Cell Biology and Physiology (H.L.), Washington University School of Medicine, St. Louis, Missouri 63110; and Department of Genetics (S.E.C., G.M.C.), Harvard Medical School, Boston, Massachusetts 02115
Address all correspondence and requests for reprints to: Richard Maas, M.D., Ph.D., Division of Genetics, Department of Medicine, Brigham & Women’s Hospital and Harvard Medical School, Thorn Building, Room 1019, 20 Shattuck Street, Boston, Massachusetts 02115. 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 genes, p57 and p15. Hoxa-10 deficiencyFS 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 periimplantation uterus.
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