EFFECTS OF POSTPUBERTAL OESTROGEN INJECTIONS ON MITOTIC ACTIVITY OF VAGINAL AND UTERINE EPITHELIAL CELLS IN MICE TREATED NEONATALLY WITH OESTROGEN

1975 ◽  
Vol 64 (1) ◽  
pp. 133-140 ◽  
Author(s):  
TAKAO MORI

SUMMARY Cell cycles of vaginal and uterine epithelial cells were studied using [3H]thymidine autoradiography in adult ovariectomized mice given oestrogen injections neonatally. The mice were in a 'persistent-oestrous' state, showing ovary-independent, continued proliferation and cornification of the vaginal epithelium. The duration of different stages of the cell cycle could not be assessed in such mice, since the percentage of labelled mitoses failed to rise to 100%. In neonatally oestrogenized, adult mice the vaginal epithelium appeared to contain a mixed population of cells. After an oestrogen injection, almost all mitoses of vaginal epithelial cells became labelled, with a generation time of about 17 h. By contrast, the generation time was about 15 h in vaginal epithelial cells of ovariectomized 'normal' mice injected with oestrogen when adult. The uterine epithelium of neonatally oestrogenized, ovariectomized mice also consisted of a mixed population of cells. A single oestrogen injection produced an increase in both the mitotic rate and cell number in the vaginal and uterine epithelium of ovariectomized 'normal' adults but not in neonatally oestrogenized, ovariectomized adults. These studies show that in mice given oestrogen neonatally, uterine and vaginal epithelial cells were not responsive to oestrogen or at least less sensitive to oestrogen than ovariectomized 'normal' controls.

2011 ◽  
Vol 55 (9) ◽  
pp. 4436-4439 ◽  
Author(s):  
Betty Wächtler ◽  
Duncan Wilson ◽  
Bernhard Hube

ABSTRACTClotrimazole and bifonazole are highly effective antifungal agents against mucosalCandida albicansinfections. Here we examined the effects of low levels of clotrimazole and bifonazole on the ability ofC. albicansto adhere, invade, and damage vaginal epithelial cells. Although adhesion and invasion were not affected, damage was greatly reduced upon azole treatment. This clearly indicates that low levels of azoles influence specific activities ofC. albicansduring distinct stages of vaginal epithelium infections.


2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Shengtao Zhou ◽  
Linjie Zhao ◽  
Tao Yi ◽  
Yuquan Wei ◽  
Xia Zhao

Abstract Women experience menopause later in life. Menopause is characterized by dramatically decreased circulating estrogen level secondary to loss of ovarian function and atrophic state of genital organs. However, the molecular mechanisms for this process are not fully understood. In this study, we aimed to investigate the potential molecular mechanisms that underlie menopause-induced uterine endometrial atrophy. Our data showed that autophagy was activated in the uterine epithelial cells of both ovariectomized rats and peri-menopausal females. Endoplasmic reticulum (ER) stress occurred even prior to autophagy induction. Integrated bioinformatics analysis revealed that ER stress induced downstream decreased release of arachidonic acid (AA) and downregulation of AA/prostaglandin E2 (PGE2) axis, which led to Akt/mTOR signaling pathway inactivation. Consequently, autophagosomes were recruited and LC3-dependent autophagy was induced in uterine epithelial cells. Treatment with exogenous E2, PGE2, salubrinal or RNAi-mediated silencing of key autophagy genes could effectively counteract estrogen depletion-induced autophagy. Collectively, autophagy is a critical regulator of the uterine epithelium that accounts for endometrial atrophy after menopause.


2006 ◽  
Vol 30 (2) ◽  
pp. 130-137
Author(s):  
Amer M. Hussin

This trail was carried out on twelve Awassi ewes in the Animal Farm of College of Veterinary Medicine in June 2005 to study the cellular changes that occur in the vaginal epithelium after parturition, by using vaginal smear method. The post-parturient period was divided into three periods; 4th, 16th and 28th days after parturition. Each period presented different sizes of vaginal epithelial cells, some of them were predominant. Keratinization takes place in all periods. The 2nd period was characterized by cellular division, presence of vacuolated epithelial cells and WBCs mainly neutrophils cells. The conclusion, variations in the vaginal epithelium may relate to the physiological status and the hormonal activity of the animals.


2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Hyunji Byun ◽  
Sojung Kwon ◽  
Kay-Uwe Wagner ◽  
Hyejin Shin ◽  
Hyunjung Jade Lim

Abstract Background The tumor susceptibility gene 101 (Tsg101), a component of the endosomal sorting complex required for transport (ESCRT) complex I, is involved in multiple biological processes involving endomembranous structures and the plasma membrane. The role of Tsg101 in the uterine epithelium was investigated in Tsg101 floxed mice crossed with Lactoferrin-iCre mice (Tsg101d/d). Methods Tsg101d/d mice were bred with stud male mice and the status of pregnancy was examined on days 4 and 6. Histological analyses were performed to examine the uterine architecture. Immunofluorescence staining of several markers was examined by confocal microscopy. Uterine epithelial cells (UECs) were isolated from Tsg101f/f and Tsg101d/d mice, and the expression of necroptosis effectors was examined by RT-PCR, western blotting, and immunofluorescence staining. UECs were also subjected to RNA expression profiling. Results Tsg101d/d female mice were subfertile with implantation failure, showing unattached blastocysts on day 6 of pregnancy. Histological and marker analyses revealed that some Tsg101d/d day 4 pregnant uteri showed a disintegrated uterine epithelial structure. Tsg101d/d UECs began to degenerate within 18 h of culture. In UECs, expression of necroptosis effectors, such as RIPK1, RIPK3, and MLKL were first confirmed. UECs responded to a stimulus to activate necroptosis and showed increased cell death. Conclusions Tsg101 deficiency in the uterine epithelium causes implantation failure, which may be caused by epithelial defects. This study provides evidence that UECs harbor a necroptotic machinery that responds to death-inducing signals. Thus, Tsg101 expression in the uterine epithelium is required for normal pregnancy in mice.


2021 ◽  
Author(s):  
Hyunji Byun ◽  
Sojung Kwon ◽  
Kay-Uwe Wagner ◽  
Hyejin Shin ◽  
Hyunjung Jade Lim

Abstract Background: The tumor susceptibility gene 101 (Tsg101), a component of the endosomal sorting complex required for transport (ESCRT) complex I, is involved in multiple biological processes involving endomembranous structures and the plasma membrane. The role of Tsg101 in the uterine epithelium was investigated in Tsg101 floxed mice crossed with Lactoferrin-iCre mice (Tsg101d/d).Methods: Tsg101d/d mice were bred with stud male mice and the status of pregnancy was examined on days 4 and 6. Histological analyses were performed to examine the uterine architecture. Immunofluorescence staining of several markers was examined by confocal microscopy. Uterine epithelial cells (UECs) were isolated from Tsg101f/f and Tsg101d/d mice, and the expression of necroptosis effectors was examined by RT-PCR, western blotting, and immunofluorescence staining. UECs were also subjected to RNA expression profiling.Results: Tsg101d/d female mice were subfertile with implantation failure, showing unattached blastocysts on day 6 of pregnancy. Histological and marker analyses revealed that some Tsg101d/d day 4 pregnant uteri showed a disintegrated uterine epithelial structure. Tsg101d/d UECs began to degenerate within 18 h of culture. In UECs, expression of necroptosis effectors, such as RIPK1, RIPK3, and MLKL were first confirmed. UECs responded to a stimulus to activate necroptosis and showed increased cell death. Conclusions: Tsg101 deficiency in the uterine epithelium causes implantation failure, which accompanies epithelial defects. This study provides evidence that UECs harbor a necroptotic machinery that responds to death-inducing signals. Thus, Tsg101 expression in the uterine epithelium is required for normal pregnancy in mice.


Author(s):  
A. C. Enders

The alteration in membrane relationships seen at implantation include 1) interaction between cytotrophoblast cells to form syncytial trophoblast and addition to the syncytium by subsequent fusion of cytotrophoblast cells, 2) formation of a wide variety of functional complex relationships by trophoblast with uterine epithelial cells in the process of invasion of the endometrium, and 3) in the case of the rabbit, fusion of some uterine epithelial cells with the trophoblast.Formation of syncytium is apparently a membrane fusion phenomenon in which rapid confluence of cytoplasm often results in isolation of residual membrane within masses of syncytial trophoblast. Often the last areas of membrane to disappear are those including a desmosome where the cell membranes are apparently held apart from fusion.


1992 ◽  
Vol 144 (1) ◽  
pp. 36-38 ◽  
Author(s):  
C.R. Murphy ◽  
P.A.W. Rogers ◽  
M.J. Hosie ◽  
J. Leeton ◽  
L. Beaton

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