title: Immunolocalization of inhibin and activin subunits in human endometrium across the menstrual cycle.
abstract: Inhibin/activin alphaC/alphaN and betaA subunits were localized immunohistochemically in the human endometrium throughout the menstrual cycle using an affinity-purified sheep polyclonal antibody raised against the alphaC/alphaN subunit and an affinity-purified rabbit polyclonal antibody raised against the betaA subunit. The betaB subunit was below the level of detection in all human endometrial samples tested. Immunoreactive inhibin alphaC/alphaN subunit was localized in the luminal epithelium, glandular epithelium, stromal tissues and vascular endothelium with no significant variation across the normal menstrual cycle. Immunoreactive betaA subunit, common to inhibin A and activins AA and AB was localized in the luminal and glandular epithelium and in migratory cells while the endometrial stromal cells, decidua, vascular smooth muscle and endothelium were devoid of immunoreactivity. A significant variation of immunoreactive betaA subunit was observed in glandular and luminal epithelium across the normal menstrual cycle. In proliferative endometrium, only a very low level of betaA immunostaining was seen in luminal and glandular epithelium, while the luminal epithelial staining increased significantly in the early secretory phase and remained relatively constant over the rest of the menstrual cycle. A progressive increase in betaA immunoreactivity was observed also in the glandular epithelium during the secretory phase reaching a maximum in the late secretory phases, and decreasing at menstruation. Co-localization studies on serial sections suggested that the migratory cells expressing strong betaA immunoreactivity were macrophages and neutrophils but not eosinophils or mast cells. Thus, cells within the human endometrium are capable of expressing inhibin/activin molecules in vivo. The variation in the pattern of secretion of the betaA subunit across the menstrual cycle suggests that activin peptides may have a physiological role in endometrial function.
authors.affiliation: Prince Henry's Institute of Medical Research, Clayton, Victoria, Australia.
authors.forename: P H
authors.initials: PH
authors.lastname: Leung
authors.forename: L A
authors.initials: LA
authors.lastname: Salamonsen
authors.forename: J K
authors.initials: JK
authors.lastname: Findlay
mesh_terms: D028341:Activins; D000818:Animals; D004717:Endometrium / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007247:Infertility, Female / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D028322:Inhibin-beta Subunits; D007265:Inhibins / Q000378:metabolism*; D008407:Mast Cells / Q000378:metabolism; D008597:Menstrual Cycle / Q000378:metabolism*; D009504:Neutrophils / Q000378:metabolism; D011817:Rabbits
chemical_list: C103008:inhibin beta A subunit; D028341:Activins; D007265:Inhibins; D028322:Inhibin-beta Subunits