scholarly journals Effects of histone deacetylase inhibitors on estradiol-induced proliferation and hyperplasia formation in the mouse uterus

2005 ◽  
Vol 185 (3) ◽  
pp. 539-549 ◽  
Author(s):  
Andrei G Gunin ◽  
Irina N Kapitova ◽  
Nina V Suslonova
Keyword(s):  
Estrogen Receptor ◽  
Histone Acetylation ◽  
Histone Deacetylase ◽  
Sodium Butyrate ◽  
Histone Deacetylase Inhibitors ◽  
Trichostatin A ◽  
Progesterone Receptors ◽  
Estrogen Receptor Α ◽  
Mouse Uterus ◽  
Myometrial Cells

It is suggested that estrogen hormones recruit mechanisms controlling histone acetylation to bring about their effects in the uterus. However, it is not known how the level of histone acetylation affects estrogen-dependent processes in the uterus, especially proliferation and morphogenetic changes. Therefore, this study examined the effects of histone deacetylase blockers, trichostatin A and sodium butyrate, on proliferative and morphogenetic reactions in the uterus under long-term estrogen treatment. Ovari-ectomized mice were treated with estradiol dipropionate (4 μg per 100 g; s.c., once a week) or vehicle and trichostatin A (0.008 mg per 100 g; s.c., once a day) or sodium butyrate (1% in drinking water), or with no additional treatments for a month. In animals treated with estradiol and trichostatin A or sodium butyrate, uterine mass was increased, and abnormal uterine glands and atypical endometrial hyperplasia were found more often. Both histone deacetylase inhibitors produced an increase in the numbers of mitotic and bromodeoxyuridine-labelled cells in luminal and glandular epithelia, in stromal and myometrial cells. Levels of estrogen receptor-α and progesterone receptors in uterine epithelia, stromal and myometrial cells were decreased in mice treated with estradiol and trichostatin A or sodium butyrate. Expression of β-catenin in luminal and glandular epithelia was attenuated in mice treated with estradiol with trichostatin A or sodium butyrate. Both histone deacetylase inhibitors have similar unilateral effects; however the action of trichostatin A was more expressed than that of sodium butyrate. Thus, histone deacetylase inhibitors exert proliferative and morphogenetic effects of estradiol. The effects of trichostatin A and sodium butyrate are associated with changes in expression of estrogen receptor-α, progesterone receptors and β-catenin in the uterus.

scholarly journals Histone Deacetylase Inhibitors Increase the Embryogenic Potential and Alter the Expression of Embryogenesis-Related and HDAC-Encoding Genes in Grapevine (Vitis vinifera L., cv. Mencía)

Plants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1164
Author(s):  
Óscar Martínez ◽  
Verónica Arjones ◽  
María Victoria González ◽  
Manuel Rey
Keyword(s):  
Vitis Vinifera ◽  
Histone Deacetylase ◽  
Sodium Butyrate ◽  
Somatic Embryos ◽  
Histone Deacetylase Inhibitors ◽  
Trichostatin A ◽  
Vitis Vinifera L ◽  
Molecular Response ◽  
Embryogenic Competence ◽  
Encoding Genes

The low induction rates of somatic embryogenesis are one of the main limitations in its routine application in the grapevine (Vitis vinifera L.). The use of an induction medium containing histone deacetylase inhibitors (trichostatin A and, mainly, sodium butyrate) resulted in an improvement of the embryogenic responses in grapevine (cv. Mencía) cotyledonary and recently germinated somatic embryos. The relative expression of several grapevine genes related to embryogenic competence or encoding histone deacetylase enzymes was studied in cotyledonary somatic embryos that were cultured in the presence of 0.5 mM sodium butyrate. The results showed a significant overexpression of the BBM and VvSERK2 genes after 24 h of culture, whereas the VvWOX2 gene was underexpressed less in treated versus untreated explants. The results suggest that the inhibitor may trigger a molecular response related to an increase in embryogenic competence and changes in the expression of associated genes. The treatment with sodium butyrate also produced significant variations in the expression of several histone deacetylase enzyme-encoding genes. These results may enhance the possibility of obtaining somatic embryos, reducing the seasonal constraints associated with the use of floral explants in grapevines.

Reciprocal Modulation of Histone Deacetylase Inhibitors Sodium Butyrate and Trichostatin A on the Energy Metabolism of Breast Cancer Cells

2015 ◽  
Vol 116 (5) ◽  
pp. 797-808 ◽  
Author(s):  
Mariana Figueiredo Rodrigues ◽  
Érika Carvalho ◽  
Paula Pezzuto ◽  
Franklin David Rumjanek ◽  
Nivea Dias Amoêdo
Keyword(s):  
Breast Cancer ◽  
Energy Metabolism ◽  
Cancer Cells ◽  
Histone Deacetylase ◽  
Sodium Butyrate ◽  
Breast Cancer Cells ◽  
Histone Deacetylase Inhibitors ◽  
Trichostatin A

Histone deacetylase inhibitors such as sodium butyrate and trichostatin A induce apoptosis through an increase of the bcl-2-related protein Bad

2001 ◽  
Vol 18 (2) ◽  
pp. 109-114 ◽  
Author(s):  
Hiroki Sawa ◽  
Hiromi Murakami ◽  
Yuko Ohshima ◽  
Toshiyuki Sugino ◽  
Takahito Nakajyo ◽  
...  
Keyword(s):  
Histone Deacetylase ◽  
Sodium Butyrate ◽  
Histone Deacetylase Inhibitors ◽  
Trichostatin A ◽  
Related Protein

Insulin-dependent transcriptional control in L6 rat myotubes is associated with modulation of histone acetylation and accumulation of the histone variant H2A.Z in the proximity of the transcriptional start site

2014 ◽  
Vol 92 (1) ◽  
pp. 61-67 ◽  
Author(s):  
Ouafa Zerzaihi ◽  
Sabrina Chriett ◽  
Hubert Vidal ◽  
Luciano Pirola
Keyword(s):  
Histone Acetylation ◽  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitors ◽  
Trichostatin A ◽  
Transcriptional Start Site ◽  
Histone Variant ◽  
Metabolic Effects ◽  
Mrna Levels ◽  
Start Site ◽  
Insulin Dependent

Besides its direct metabolic effects, insulin induces transcriptional alterations in its target tissues. However, whether such changes are accompanied by epigenetic changes on the chromatin template encompassing insulin responsive genes is unclear. Here, mRNA levels of insulin-responsive genes hexokinase 2 (Hk2), insulin receptor substrate (Irs2), and the PI3K subunit p85β (Pik3r2) were compared in control versus insulin-stimulated L6 myotubes. Chromatin immunoprecipitation (ChIP) was performed with antibodies directed to histone H2A, histone variant H2A.Z, acetylated histone H3 on lysines 9/14, and acetylated H2A.Z. Insulin induced a more than 2-fold Hk2 mRNA increase, while Irs2 and Pik3r2 were downregulated. ChIP to H2A and H2A.Z showed higher H2A.Z accumulation around the transcriptional start site (TSS) of these insulin-modulated genes, while H2A.Z accumulation was lower distally to the TSS in the Hk2 promoter. H2A.Z levels and H3K9/14 acetylation correlated on several loci along the Hk2 gene, and H3K9/14 as well as H2A.Z acetylation was enhanced by insulin treatment. On the contrary, reduced H3K9/14 acetylation was observed in insulin-repressed Irs2 and Pik3r2, and recovery of acetylation by treatment with the histone deacetylase inhibitor trichostatin A reverted insulin-induced Irs2 downregulation. The chromatin regions encompassing selected insulin-responsive genes are thus featured by accumulation of H2A.Z around the TSS. H2A.Z accumulation facilitates insulin-dependent modulation of pharmacologically treatable H3K9/14 and H2A.Z acetylations. Indeed, inhibition of histone deacetylases by TSA treatment reverted insulin induced Irs2 gene downregulation. Dysregulated histone acetylation may thus be potentially targeted with histone deacetylase inhibitors.

Regulation of HOXA10 expression by phytoestrogens

2007 ◽  
Vol 292 (2) ◽  
pp. E435-E442 ◽  
Author(s):  
G. Eda Akbas ◽  
Xiaolan Fei ◽  
Hugh S. Taylor
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
In Utero ◽  
Estrogen Response Element ◽  
Mouse Uterus ◽  
Response Element ◽  
Estrogen Response ◽  
Uterine Anomalies ◽  
Mrna And Protein Expression ◽  
Adult Exposure

HOXA10 is necessary for normal development of the Müllerian duct, and continued adult expression in the uterus is necessary for female fertility. HOXA10 expression is altered by diethylstilbestrol, leading to uterine anomalies. Other endocrine disruptors may potentially lead to reproductive anomalies or dysfunction by altering HOXA10 expression. Here we investigated the effect of isoflavones on HOXA10 expression after in utero or adult exposure in the mouse. Genistein, but not diadzein, regulated HOXA10 mRNA and protein expression in the adult mouse uterus. In contrast, in utero genistein or diadzein exposure had no lasting effect on HOXA10 expression in the exposed offspring. Reporter gene expression driven by the HOXA10 estrogen response element was increased in a dose-responsive manner by genistein, but not daidzein. Neither estrogen receptor-α nor estrogen receptor-β binding to the HOXA10 estrogen response element was affected by genistein or daidzein. In utero exposure to isoflavones is unlikely to result in HOXA10-mediated developmental anomalies. Adult genistein exposure alters uterine HOXA10 expression, a potential mechanism by which this agent affects fertility.

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