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Characterization of the expression and steroid hormone control of sialomucin complex in the rat uterus: Implications for uterine receptivity
Author(s) -
McNeer Richard R.,
Carraway Coralie A. Carothers,
Fregien Nevis L.,
Carraway Kermit L.
Publication year - 1998
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199807)176:1<110::aid-jcp13>3.0.co;2-b
Subject(s) - uterus , endocrinology , biology , medicine , endometrium , estrogen , mammary gland , microbiology and biotechnology , cancer , breast cancer
The sialomucin complex (SMC), originally isolated as a heterodimeric glycoprotein complex from membranes of ascites sublines of a highly metastatic mammary adenocarcinoma, consists of a high M r mucin subunit (ASGP‐1, ascites sialoglycoprotein) and a transmembrane subunit (ASGP‐2) with two epidermal growth factor‐like domains. SMC has been characterized in the mammary gland, where it is present in both membrane and nonmembrane (soluble) forms, the latter lacking its transmembrane domain. SMC in the mammary gland is observed during pregnancy and lactation, but not in the virgin gland, and is regulated by a posttranscriptional mechanism. Both membrane and nonmembrane forms of SMC are found in rat uterus, also as a complex of ASGP‐1 and ASGP‐2. Immunocytochemical analyses indicate that the primary site of expression is at the luminal surface of the endometrium. Approximately 40% of the SMC, corresponding to the nonmembrane fraction, is removed by rinsing uterine preparations with saline, indicating that the soluble form is adsorbed loosely to the cell surface. In contrast to mammary gland, SMC is most highly expressed in the virgin animal, and its expression varies during the estrous cycle with the steady state level of transcript. The complex is present in a location consistent with steric inhibition of blastocyst implantation and is abruptly lost at the beginning of the period of receptivity for implantation. Expression of SMC in the uterus is regulated by estrogen and progesterone and is inversely correlated with receptivity. Both implantation and loss of SMC expression can be blocked with RU486. We propose that the downregulation of SMC and its loss from the apical surface of the rat uterine lining contribute to the generation of the receptive state for uterine implantation. Furthermore, the presence of both membrane and soluble SMC at the luminal surface of the endometrium may provide a model for its proposed protective function in other accessible and vulnerable epithelia. J. Cell. Physiol. 176:110–119, 1998. © 1998 Wiley‐Liss, Inc.