Action of epidermal chalone on 17-?-estradiol-stimulated proliferation of vaginal epithelial cells of ovariectomized mice

1984 ◽  
Vol 98 (4) ◽  
pp. 1425-1426
Author(s):  
K. M. Svitkova ◽  
S. A. Ketlinskii

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.



2021 ◽  
Vol 143 ◽  
pp. 103253
Author(s):  
Matthew William Woods ◽  
Muhammad Atif Zahoor ◽  
Jeffrey Lam ◽  
Puja Bagri ◽  
Haley Dupont ◽  
...  


2011 ◽  
Vol 92 (9) ◽  
pp. 1981-1993 ◽  
Author(s):  
Xiao-Dan Yao ◽  
Kenneth Lee Rosenthal

Viruses that establish persistent infections have evolved numerous strategies to evade host innate antiviral responses. We functionally assessed the role of herpes simplex virus type 2 (HSV-2) virion host shutoff (vhs) protein on innate immune sensing pathways in human vaginal epithelial cells (VK2 ECs). Infection of cells with wild-type (WT) HSV-2 significantly decreased expression of innate immune sensors of viral infection, Toll-like receptor (TLR)2, TLR3, retinoic acid inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (Mda-5), relative to cells infected with a mutant that lacks vhs (vhsB) or mock-infected cells. Transfection with HSV-2 vhs similarly decreased expression of TLR2, TLR3, RIG-I and Mda-5, which was also confirmed in human embryonic kidney (HEK) 293 cells. vhsB infection of VK2 cells caused robust increases in the active form of interferon regulatory factor (IRF)3 and its translocation to the nucleus compared with the WT. Additionally, IRF3 activation by Sendai virus and polyinosinic : polycytidylic acid-induced stimulation of beta interferon (IFN-β) was significantly inhibited in vhs-transfected cells. Overall, our findings provide the first evidence that HSV-2 vhs plays roles in selectively inhibiting TLR3 and RIG-I/Mda-5, as well as TLR2-mediated antiviral pathways for sensing dsRNA and effectively suppresses IFN-β antiviral responses in human vaginal ECs.







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