scholarly journals Trichomonas vaginalis: Dehydroepiandrosterone sulfate and 17β-estradiol alter NTPDase activity and gene expression

2010 ◽  
Vol 125 (3) ◽  
pp. 187-195 ◽  
Author(s):  
Caroline Rückert ◽  
Cristiane dos Santos Stuepp ◽  
Barbara Gottardi ◽  
Jessica Rosa ◽  
Julia Cisilotto ◽  
...  
PLoS ONE ◽  
2016 ◽  
Vol 11 (9) ◽  
pp. e0161430 ◽  
Author(s):  
Winfred Stacey ◽  
Shreyas Bhave ◽  
Rosalie M. Uht
Keyword(s):  

PLoS ONE ◽  
2011 ◽  
Vol 6 (12) ◽  
pp. e28402 ◽  
Author(s):  
Jata Shankar ◽  
Thomas D. Wu ◽  
Karl V. Clemons ◽  
Jomar P. Monteiro ◽  
Laurence F. Mirels ◽  
...  

Endocrinology ◽  
2001 ◽  
Vol 142 (3) ◽  
pp. 1000-1008 ◽  
Author(s):  
Ismael Samudio ◽  
Carrie Vyhlidal ◽  
Fan Wang ◽  
Matthew Stoner ◽  
Ichen Chen ◽  
...  

2002 ◽  
Vol 13 (10) ◽  
pp. 3720-3729 ◽  
Author(s):  
Maria Marino ◽  
Filippo Acconcia ◽  
Francesco Bresciani ◽  
Alessandro Weisz ◽  
Anna Trentalance

Estrogens induce cell proliferation in target tissues by stimulating progression through the G1 phase of the cell cycle. Activation of cyclin D1 gene expression is a critical feature of this hormonal action. The existence of rapid/nongenomic estradiol-regulated protein kinase C (PKC-α) and extracellular signal-regulated kinase (ERK) signal transduction pathways, their cross talk, and role played in DNA synthesis and cyclin D1 gene transcription have been studied herein in human hepatoma HepG2 cells. 17β-Estradiol was found to rapidly activate PKC-α translocation and ERK-2/mitogen-activated protein kinase phosphorylation in this cell line. These actions were independent of each other, preceding the increase of thymidine incorporation into DNA and cyclin D1expression, and did not involve DNA binding by estrogen receptor. The results obtained with specific inhibitors indicated that PKC-α pathway is necessary to mediate the estradiol-induced G1-S progression of HepG2 cells, but it does not exert any effect(s) on cyclin D1 gene expression. On the contrary, ERK-2 cascade was strongly involved in both G1-S progression and cyclin D1gene transcription. Deletion of its activating protein-1 responsive element motif resulted in attenuation of cyclin D1 promoter responsiveness to estrogen. These results indicate that estrogen-induced cyclin D1 transcription can occur in HepG2 cells independently of the transcriptional activity of estrogen receptor, sustaining the pivotal role played by nongenomic pathways of estrogen action in hormone-induced proliferation.


2006 ◽  
Vol 99 (1) ◽  
pp. 209-220 ◽  
Author(s):  
Wan Ru Lee ◽  
Chien-Cheng Chen ◽  
Shengxi Liu ◽  
Stephen Safe

2010 ◽  
Vol 1307 ◽  
pp. 28-42 ◽  
Author(s):  
Nigel C. Noriega ◽  
Dominique H. Eghlidi ◽  
Vasilios T. Garyfallou ◽  
Steven G. Kohama ◽  
Sharon G. Kryger ◽  
...  

2020 ◽  
Vol 117 (23) ◽  
pp. 13033-13043
Author(s):  
Ayelen Lizarraga ◽  
Zach Klapholz O’Brown ◽  
Konstantinos Boulias ◽  
Lara Roach ◽  
Eric Lieberman Greer ◽  
...  

Trichomonas vaginalisis a common sexually transmitted parasite that colonizes the human urogenital tract causing infections that range from asymptomatic to highly inflammatory. Recent works have highlighted the importance of histone modifications in the regulation of transcription and parasite pathogenesis. However, the nature of DNA methylation in the parasite remains unexplored. Using a combination of immunological techniques and ultrahigh-performance liquid chromatography (UHPLC), we analyzed the abundance of DNA methylation in strains with differential pathogenicity demonstrating that N6-methyladenine (6mA), and not 5‐methylcytosine (5mC), is the main DNA methylation mark inT. vaginalis. Genome-wide distribution of 6mA reveals that this mark is enriched at intergenic regions, with a preference for certain superfamilies of DNA transposable elements. We show that 6mA inT. vaginalisis associated with silencing when present on genes. Interestingly, bioinformatics analysis revealed the presence of transcriptionally active or repressive intervals flanked by 6mA-enriched regions, and results from chromatin conformation capture (3C) experiments suggest these 6mA flanked regions are in close spatial proximity. These associations were disrupted when parasites were treated with the demethylation activator ascorbic acid. This finding revealed a role for 6mA in modulating three-dimensional (3D) chromatin structure and gene expression in this divergent member of the Excavata.


2006 ◽  
Vol 231 (3) ◽  
pp. 311-316 ◽  
Author(s):  
Toshinobu Hatsumi ◽  
Yutaka Yamamuro

The biological actions of estrogen are mostly conveyed through interaction with the nuclear estrogen receptor (ER). Previous evidence indicated that estrogen participates in self-regulation through the modulation of the expression of its own receptors. However, the self-regulation of estrogen against ER in the mammary gland during established lactation has not yet been investigated. The present study evaluated ER gene expression in the lactating gland activated by large doses of 17β-estradiol (E2). Repeated E2 treatments dose-dependently decreased the gene, expression of ER, especially its subtype ER-α mRNA, Which was decreased to 10% of the vehicle-injected control by 1 μg E2 injection, whereas it was decreased by 73% for another subtype, ER-β. A single injection of 5 μg of E2 drastically downregulated both ER genes within 12 hrs of injection, and they did not recover to pretreatment level within 48 hrs. Western blot analysis verified that E2 treatment inhibited the phosphorylation of Stat5, which is a potent transcriptional regulator for ER mRNA. The present findings demonstrate that E2 treatment decreases the gene expression of its own receptor in the mammary gland during galactopoesis and induces an apparent transition of the ER profile in the mammary gland during lactation into postlactation.


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