title: Increased incidence of apoptosis in non-labour-affected cytotrophoblast cells in term fetal membranes overlying the cervix.
abstract: A regional reduction in the cellularity of the cytotrophoblastic and decidual layers occurs in the fetal membranes overlying the cervix in the lower uterine segment prior to labour. Although the mechanism(s) involved are not known it could result from regionally increased apoptosis, the histological manifestation of programmed cell death, or decreased proliferation. Apoptosis was assessed in regionally sampled fetal membranes from women undergoing elective Caesarean section (n = 14) by the presence of apoptotic bodies by light and electron microscopy. Cell proliferation was assessed by immunocytochemical detection of the protein Ki-67. Apoptotic bodies were identified in all regions of the fetal membrane with the highest incidence found within the cytotrophoblast layer. However, this layer in fetal membranes biopsied over the cervix contained significantly more apoptotic bodies (mean +/- SD 0.085 +/- 0.020%) compared to the layer in fetal membranes obtained from the mid-zone (0.020 +/- 0.008%) apoptotic bodies. Isolated Ki-67 positive cells were detected in the cytotrophoblast layer, but no regional differences in their incidence were seen. Fetal membranes also failed to exhibit significant immunoreactivity for BCL-2 but exhibited strong BAX immunoreactivity within the decidual layer. We conclude that the regionally increased incidence of apoptosis in the cytotrophoblastic layer in the membrane overlying the cervix may account for the reduction in its cellularity but not the relative decrease in the decidual layer. Given the consequence of the loss of local function in degrading uterotonins and stabilizing the fetal membrane, the study of the regulation of apoptosis in these cells may have important implications for fetal membrane rupture and parturition.
authors.affiliation: Preterm Birth Research Group, Department of Obstetrics & Gynaecology, University of Leicester, Clinical Sciences Building, Leicester Royal Infirmary, P. O. Box 65, Leicester LE2 7LX, UK.
authors.forename: J
authors.initials: J
authors.lastname: McLaren
authors.forename: D J
authors.initials: DJ
authors.lastname: Taylor
authors.forename: S C
authors.initials: SC
authors.lastname: Bell
mesh_terms: D000650:Amnion / Q000166:cytology; D017209:Apoptosis; D002455:Cell Division; D002584:Cervix Uteri; D002585:Cesarean Section; D003239:Connective Tissue Cells; D003656:Decidua / Q000166:cytology; D004847:Epithelial Cells; D005321:Extraembryonic Membranes / Q000166:cytology*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000032:analysis; D008854:Microscopy, Electron; D011247:Pregnancy; D011518:Proto-Oncogene Proteins / Q000032:analysis; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000032:analysis; D014327:Trophoblasts / Q000166:cytology*; D051028:bcl-2-Associated X Protein
chemical_list: C494826:BAX protein, human; D019394:Ki-67 Antigen; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein