During implantation in mice, tissue inhibitor of matrix metalloproteinases‐3 is believed to play a key role in inhibiting matrix metalloproteinase activity associated with embryo invasion and tissue remodeling. The first objective of this study was to quantitatively compare the steady‐state mRNA levels of tissue inhibitors of matrix metalloproteinases between segments of the mouse uterus undergoing decidualization compared to those that are not during early pregnancy plus oil‐induced decidualization. Steady‐state tissue inhibitor of metalloproteinase‐3 mRNA levels were significantly greater in implantation compared to interimplantation areas on days 6 and 7 of pregnancy and in stimulated compared to nonstimulated uterine horns at 48 and 72 hr after artificial induction of decidualization. Steady‐state tissue inhibitor of metalloproteinase‐1 mRNA levels were significantly greater in implantation compared to interimplantation areas on days 5–8 of pregnancy and in stimulated compared to nonstimulated uterine horns at 24, 48, and 72 hr after oil stimulation. Therefore, the steady‐state mRNA levels of tissue inhibitors of metalloproteinase‐1 and ‐3 increased in the uterus during decidualization. The second objective of this study was to determine if transforming growth factor‐β1 influences tissue inhibitors of metalloproteinase mRNA concentrations in mouse endometrial stromal cells. As determined by Northern blot analyses, transforming growth factor β1 significantly increased tissue inhibitors of matrix metalloproteinases‐1 and ‐3 mRNA levels in cultured mouse endometrial stromal cells isolated from uteri sensitized for decidualization. On the other hand, interleukin‐1, epidermal growth factor, and leukemia inhibitory factor had no effect. The results of this study further characterize the tissue inhibitor of metalloproteinase expression in the uterus during implantation and artificially induced decidualization and the potential control of their expression in the stroma by transforming growth factor. Mol. Reprod. Dev. 59:159–167, 2001. © 2001 Wiley‐Liss, Inc.