Both stressors and novel male exposure can disrupt intrauterine implantation of fertilized ova in inseminated female mice. Adhesion molecules including e-cadherin support blastocyst implantation by promoting their binding to the uterine epithelium and closure of the uterine lumen around blastocysts. We compared inseminated females that were each exposed to a rat across a wire-mesh grid to control females that were left undisturbed during gestation days (GD) 1 to 5. On GD 6, the number of implantation sites was significantly reduced in the rat-stressed females, and 17β-estradiol levels were elevated and progesterone levels were suppressed in females showing implantation failure1. Uterine luminal area was significantly greater and e-cadherin levels were significantly reduced in rat-stressed females. We subsequently compared females exposed to novel males and isolated control females during GD 2 to 8, observing a significant reduction in implantation sites in male-exposed females compared to controls2. Uterine luminal area was greater in male-exposed females than in controls during the post-implantation period (GD 5 to 7). E-cadherin levels were suppressed by male exposure during GD 4 to 7. As estradiol suppresses e-cadherin and progesterone promotes e-cadherin, these data are consistent with a role of a high ratio of estradiol to progesterone in both stress-induced and male-exposure-induced implantation failure.