Activation of telomerase by seminal plasma in malignant and normal cervical epithelial cells

2011 ◽  
Vol 225 (2) ◽  
pp. 203-211 ◽  
Author(s):  
Li Liu ◽  
Cheng Liu ◽  
Fenglan Lou ◽  
Guiyu Zhang ◽  
Xizhi Wang ◽  
...  
2004 ◽  
Vol 16 (9) ◽  
pp. 229 ◽  
Author(s):  
D. J. Sharkey ◽  
S. A. Robertson

Exposure to semen at intercourse in women elicits an inflammation-like response characterised by recruitment of inflammatory cells and expression of pro-inflammatory cytokines including GM-CSF, interleukin-6 (IL-6) and IL-8 (1). Studies in animal models have implicated TGFβ as the major active moiety in seminal plasma, and we have shown previously that TGFβ1 and TGFβ3 are present in high concentrations in human seminal plasma (>100 ng/mL), while TGFβ2 is less abundant. To investigate the physiological significance of each of the three TGFβ isoforms as pro-inflammatory agents in human seminal plasma, we have established in vitro model systems to measure human cervical cell cytokine synthesis. Primary cervical epithelial cells prepared from ectocervix of hysterectomy tissues or transformed Ect1 cells were incubated for 12 h with human recombinant TGFβ (isoforms 1, 2 or 3) or with seminal plasma in the presence or absence of isoform-specific TGFβ neutralising antibodies. Epithelial cell supernatants were recovered 24 h later and supernatants were analysed by commercial ELISA to quantify GM-CSF, IL-6 and IL-8 production. Each of the three TGFβ isoforms mimicked seminal plasma and were comparable in their capacity to stimulate >10-fold increases in both GM-CSF and IL-6 expression in a dose-responsive manner. In contrast, unlike seminal plasma none of the TGFβ isoforms induced IL-8 expression. Addition of neutralising antibodies to TFGβ1, TGFβ2 and TGFβ3 each effected >50% reduction in the ability of seminal plasma to induce GM-CSF and IL-6, but did not impair seminal plasma-stimulated IL-8 production. Together these data show that TGFβ1, TGFβ2 and TGFβ3 are major active constituents of seminal plasma, acting to elicit GM-CSF and IL-6 production in cervical epithelial cells. However, TGFβ does not fully account for the pro-inflammatory effects of human seminal plasma, and other active constituents remain to be identified. (1) D. J. Sharkey et al. (2003) Proc. SRB.


2009 ◽  
Vol 199 (2) ◽  
pp. 227-235 ◽  
Author(s):  
Adam J. Potter ◽  
Stephen P. Kidd ◽  
Jennifer L. Edwards ◽  
Megan L. Falsetta ◽  
Michael A. Apicella ◽  
...  

Gene Reports ◽  
2022 ◽  
Vol 26 ◽  
pp. 101456
Author(s):  
Abbas Hadi Albosale ◽  
Olga Andreevna Garbuzova ◽  
Konstantin Alekseevich Kovalenko ◽  
Elena Vladimirovna Mashkina

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Jennifer Couret ◽  
Carley Tasker ◽  
Jaeha Kim ◽  
Tiina Sihvonen ◽  
Saahil Fruitwala ◽  
...  

Reproduction ◽  
2021 ◽  
Author(s):  
Ourlad Alzeus Gaddi Tantengco ◽  
Talar Kechichian ◽  
Kathleen L Vincent ◽  
Richard B Pyles ◽  
Paul Mark B Medina ◽  
...  

Ureaplasma parvum is a commensal bacterium in the female reproductive tract but has been associated with pregnancy complications such as preterm prelabor rupture of membranes and preterm birth (PTB). However, the pathologic effects of U. parvum in the cervix, that prevents ascending infections during pregnancy, are still poorly understood. To determine the impact of U. parvum on the cervix, ectocervical (ecto) and endocervical (endo) epithelial and stromal cells were incubated with U. parvum. Macrophages were also tested as a proxy for cervical macrophages to determine the antigenicity of U. parvum. The effects of U. parvum, including influence on cell cycle and cell death, antimicrobial peptide production, epithelial-to-mesenchymal transition (EMT), and inflammatory cytokine levels, were assessed. U. parvum colonized cervical epithelial and stromal cells 4 hours post-infection. Like uninfected control, U. parvum neither inhibited cell cycle progression and nor caused cell death in cervical epithelial and stromal cells. U. parvum increased the production of the antimicrobial peptides (AMPs) cathelicidin and human β-defensin 3 and exhibited weak signs of EMT evidenced by decreased cytokeratin 18 and increased vimentin expression in cervical epithelial cells. U. parvum induced a pro-inflammatory environment (cytokines) and increased MMP-9 in cervical epithelial cells but promoted pro- and anti-inflammatory responses in cervical stromal cells and macrophages. U. parvum may colonize the cervical epithelial layer, but induction of AMPs and anti-inflammatory response may protect the cervix and may prevent ascending infections that can cause PTB. These findings suggest that U. parvum is a weak inducer of inflammation in the cervix.


1994 ◽  
Vol 68 (2) ◽  
pp. 1173-1178 ◽  
Author(s):  
M Chen ◽  
N Popescu ◽  
C Woodworth ◽  
Z Berneman ◽  
M Corbellino ◽  
...  

1994 ◽  
Vol 58 (5) ◽  
pp. 713-720 ◽  
Author(s):  
Jie Zheng ◽  
Torsten Wahlström ◽  
Jorma Paavonen ◽  
Antti Vaheri

1993 ◽  
Vol 4 (6) ◽  
pp. 342-345 ◽  
Author(s):  
S L Patrick ◽  
T C Wright ◽  
H E Fox ◽  
H S Ginsberg

Women are infected with HIV in increasing numbers; the predominant mode of spread is through heterosexual transmission. Little is known regarding the mechanism of HIV transit through the female genital tract. We investigated whether early passaage cervical epithelial cells could be directly infected with HIV-1LAI*. Virus production was measured using the reverse transcriptase (RT) assay and direct assay for syncytia-forming units. In-situ hybridization was performed on infected cervical cell cultures. Immunostaining was carried out using a monoclonal antibody to leukocyte common antigen (LCA). Virus was recovered in the supernatants of all infected cervical cultures. Localization of HIV infection using in-situ hybridization identified rare cells in the population which gave a strong signal. These infected cells had a lymphoid morphology and were also detected using immunostaining for LAC. Cervical epithelial cells were uninfected in this in vitro model; cells in this population which supported viral replication were most likely of the macrophage/monocyte lineage.


1991 ◽  
Vol 36 (10) ◽  
pp. 737-745 ◽  
Author(s):  
J.C. Farges ◽  
M.L. Couble ◽  
A. Joffre ◽  
D.J. Hartmann ◽  
H. Magloire

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