Mucin (Muc-1) expression is differentially regulated in uterine luminal and glandular epithelia of the baboon (Papio anubis).

Changes in the organization and composition of apical cell surface glycoconjugates accompany the transition of luminal epithelial cells from the prereceptive state of the uterus in many species. In spite of the biological and clinical significance of this process, few molecular markers have arisen as useful predictors of uterine receptivity. Recent studies in mice demonstrate that the transmembrane mucin glycoprotein, Muc-1, is abundantly expressed at the apical surface of luminal epithelia under most conditions and is invariably reduced in receptive uteri. These and other observations have led to the suggestion that mucins serve an antiadhesive role and function to maintain a nonreceptive uterine state. A pan-species Muc-1 specific antibody recognizing a peptide motif conserved in the cytoplasmic domain of Muc-1 was used to examine the temporal and spatial expression of cell-associated Muc-1 in baboon uteri under a variety of conditions, including the pre- and perimplantation periods. Muc-1 expression was not driven by estrogen influences alone, but required progesterone action. In animals exposed to both steroids, Muc-1 was expressed at low moderate levels in epithelia of the basalis and functionalis regions. The highest expression of Muc-1 was detected in surface epithelium of the preimplantation phase, i.e., up to Day 8 (Day 0 = day of ovulation), or in ovariectomized animals receiving a steroid hormone regime that mimicked this phase (14 days of estrogen priming followed by 7 days of estrogen plus progesterone). Continued exposure to both hormones, i.e., as seen at Days 10-12 or in ovariectomized baboons given 14 days of estrogen plus progesterone treatment after estrogen priming, resulted in marked reduction of Muc-1 expression in the surface epithelium; however, staining patterns in the glandular epithelium were unchanged by this treatment. The expression of Muc-1 on the surface epithelium during the prereceptive phase was associated with the presence of both estrogen and progestin receptors in these epithelia. Muc-1 expression was reduced by neither antiestrogen treatment during the prereceptive stage nor antiprogestin treatment through to the receptive phase. Furthermore, persistent Muc-1 expression in the functionalis and basalis epithelium correlated with expression of progestin receptors. Thus, Muc-1 expression appeared to be progesterone-dependent rather than estrogen-dependent. It is concluded that Muc-1 expression in surface epithelium serves as a marker of the prereceptive phase in the baboon and that loss of Muc-1 from surface epithelium correlates with generation of a receptive uterine state.