Influence of 17β-Estradiol on Gene Expression of Paracoccidioides during Mycelia-to-Yeast Transition

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.

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17β-estradiol (E2) induces cdc25A gene expression in breast cancer cells by genomic and non-genomic pathways

Journal of Cellular Biochemistry ◽

10.1002/jcb.20902 ◽

2006 ◽

Vol 99 (1) ◽

pp. 209-220 ◽

Cited By ~ 15

Author(s):

Wan Ru Lee ◽

Chien-Cheng Chen ◽

Shengxi Liu ◽

Stephen Safe

Keyword(s):

Breast Cancer ◽

Gene Expression ◽

Cancer Cells ◽

Breast Cancer Cells ◽

17Β Estradiol

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Influence of 17β-estradiol and progesterone on GABAergic gene expression in the arcuate nucleus, amygdala and hippocampus of the rhesus macaque

Brain Research ◽

10.1016/j.brainres.2009.10.011 ◽

2010 ◽

Vol 1307 ◽

pp. 28-42 ◽

Cited By ~ 23

Author(s):

Nigel C. Noriega ◽

Dominique H. Eghlidi ◽

Vasilios T. Garyfallou ◽

Steven G. Kohama ◽

Sharon G. Kryger ◽

...

Keyword(s):

Gene Expression ◽

Rhesus Macaque ◽

Arcuate Nucleus ◽

17Β Estradiol

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0845 Effect of 17β-estradiol on milk production, hormone secretion, and mammary gland gene expression of dairy cows

Journal of Animal Science ◽

10.2527/jam2016-0845 ◽

2016 ◽

Vol 94 (suppl_5) ◽

pp. 406-407

Author(s):

J. J. Tong ◽

I. M. Thompson ◽

P. Lacasse

Keyword(s):

Gene Expression ◽

Mammary Gland ◽

Dairy Cows ◽

Milk Production ◽

Hormone Secretion ◽

17Β Estradiol

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Downregulation of Estrogen Receptor Gene Expression by Exogenous 17β-Estradiol in the Mammary Glands of Lactating Mice

Experimental Biology and Medicine ◽

10.1177/153537020623100311 ◽

2006 ◽

Vol 231 (3) ◽

pp. 311-316 ◽

Cited By ~ 25

Author(s):

Toshinobu Hatsumi ◽

Yutaka Yamamuro

Keyword(s):

Gene Expression ◽

Estrogen Receptor ◽

Mammary Gland ◽

Single Injection ◽

Receptor Gene ◽

Self Regulation ◽

Estrogen Receptor Gene ◽

17Β Estradiol ◽

Nuclear Estrogen Receptor ◽

Receptor Gene Expression

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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17β-Estradiol decreases hypoxic induction of erythropoietin gene expression

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00573.2001 ◽

2002 ◽

Vol 283 (2) ◽

pp. R496-R504 ◽

Cited By ~ 32

Author(s):

Harshini Mukundan ◽

Thomas C. Resta ◽

Nancy L. Kanagy

Keyword(s):

Gene Expression ◽

Nitric Oxide ◽

Oxygen Delivery ◽

Chronic Hypoxia ◽

No Synthase ◽

No Production ◽

Enos Expression ◽

Hypoxic Induction ◽

Endothelial No Synthase ◽

17Β Estradiol

Exposure to chronic hypoxia induces erythropoietin (EPO) production to facilitate oxygen delivery to hypoxic tissues. Previous studies from our laboratory found that ovariectomy (OVX) exacerbates the polycythemic response to hypoxia and treatment with 17β-estradiol (E2-β) inhibits this effect. We hypothesized that E2-β decreases EPO gene expression during hypoxia. Because E2-β can induce nitric oxide (NO) production and NO can attenuate EPO synthesis, we further hypothesized that E2-β inhibition of EPO gene expression is mediated by NO. These hypotheses were tested in OVX catheterized rats treated with E2-β (20 μg/day) or vehicle for 14 days and exposed to 8 or 12 h of hypoxia (12% O2) or normoxia. We found that E2-β treatment significantly decreased EPO synthesis and gene expression during hypoxia. E2-β treatment did not induce endothelial NO synthase (eNOS) expression in the kidney but potentiated hypoxia-induced increases in plasma nitrates. We conclude that E2-β decreases hypoxic induction of EPO. However, this effect does not appear to be related to changes in renal eNOS expression.

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