Identification of Estrogen-Responsive Genes in Neuroblastoma SK-ER3 Cells

Garnier, Martine; Lorenzo, Diego Di; Albertini, Alberto; Maggi, Adriana

doi:10.1523/jneurosci.17-12-04591.1997

Cited by 64 publications

(44 citation statements)

References 60 publications

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“…This increase was not observed with the antiestrogen TOT. Similarly Garnier et al, using differential display report that PTa mRNA expression was also enhanced in neuroblastoma cells after estrogen treatment (Garnier et al, 1997). The present studies now show that the increase in PTa mRNA in the presence of E 2 is also evident at the protein level.…”

Section: Discussionsupporting

confidence: 84%

“…Their studies indicate the involvement of two half-EREs in the regulation by estrogens. These halfEREs, located at 7886 to 7861 and 7588 to 7560, were also proposed (but not examined) by Garnier et al (1997) to be involved in estrogen regulation of PTa expression in neuroblastoma cells. While mutational analyses support the involvement of these two halfEREs (Martini and Katzenellenbogen, 2001), the halfEREs were not cloned upstream of a heterologous promoter to indicate enhancer activity.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, deletion of the E-box did not affect E 2 -mediated upregulation of PTa gene transcriptional activity. Another group has shown that E 2 does not regulate the expression of N-myc, the neural counterpart of c-myc in neural cells, wherein E 2 has been demonstrated to upregulate PTa expression (Garnier et al, 1997). Additional supporting evidence for direct transcriptional regulation of the PTa gene by the ER is that the increase in PTa expression was observed 1 h after estrogen treatment in neuroblastoma cells (Garnier et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

“…While there are reports of ER binding to half-EREs, there are also reports of binding of other transcription factors to the half-ERE that results in the regulation of ER-mediated gene transcription (Chen et al, 1998;Garnier et al, 1997;Klinge et al, 1997). Also of interest are three repeats of a TGCCC element in this region, one next to the half-ERE and two sequentially ordered at the 3' end ( Figure 3c).…”

Section: Identification Of Pta Gene Promoter Regions Required For Actmentioning

confidence: 99%

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Regulation of prothymosin α by estrogen receptor α: molecular mechanisms and relevance in estrogen-mediated breast cell growth

Bianco

Montano

2002

Oncogene

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Prothymosin a (PTa) is a small highly acidic protein found in the nuclei of virtually all mammalian tissues. Its high conservation in mammals and wide tissue distribution suggest an essential biological role. While the exact mechanism of action of PTa remains elusive, the one constant has been its relationship with the proliferative state of the cell and its requirement for cellular growth and survival. Recently PTa was found to promote transcriptional activity by sequestering the anticoactivator, REA from the Estrogen Receptor (ER) complex. We now report that Estradiol (E 2 ) upregulates PTa mRNA and protein expression. Further studies indicate that ERa regulates PTa gene transcriptional activity. We have also delimited the region of PTa gene promoter involved in ERa-mediated transcriptional regulation and identified a novel ERabinding element. Increased intracellular PTa expression in the presence of estrogens is accompanied by increased nuclear/decreased cytoplasmic localization. Increased nuclear expression of PTa is correlated with increased proliferation as measured by expression of Ki67 nuclear antigen. Conversely, inhibition of nuclear PTa expression in breast cancer cells using antisense methodology resulted in the inhibition of E 2 -induced breast cancer cell proliferation. Overall these studies underscore the importance of PTa in estrogen-induced breast cell proliferation.

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Section: Discussionsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Identification Of Pta Gene Promoter Regions Required For Actmentioning

confidence: 99%

See 2 more Smart Citations

Regulation of prothymosin α by estrogen receptor α: molecular mechanisms and relevance in estrogen-mediated breast cell growth

Bianco

Montano

2002

Oncogene

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“…Many experimental studies examined the responsiveness of DA neurons to estrogens and showed that estradiol levels induces DA synthesis and release, as well as DA neurons differentiation ( [57,58,81,151,171]). Importantly, MPTP caused greater DA depletion in male compared with female mice [59]; moreover, treatment with estradiol prevented the reduction in DA concentrations and the activation of glia in the striatum of animals treated with MPTP ( [31,59,169,235]).…”

Section: Estrogens and Parkinson's Diseasementioning

confidence: 99%

Estrogen anti-inflammatory activity in brain: A therapeutic opportunity for menopause and neurodegenerative diseases

Vegeto

Benedusi

Maggi

2008

Frontiers in Neuroendocrinology

271

206

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a b s t r a c tRecent studies highlight the prominent role played by estrogens in protecting the central nervous system (CNS) against the noxious consequences of a chronic inflammatory reaction. The neurodegenerative process of several CNS diseases, including Multiple Sclerosis, Alzheimer's and Parkinson's Diseases, is associated with the activation of microglia cells, which drive the resident inflammatory response. Chronically stimulated during neurodegeneration, microglia cells are thought to provide detrimental effects on surrounding neurons. The inhibitory activity of estrogens on neuroinflammation and specifically on microglia might thus be considered as a beneficial therapeutic opportunity for delaying the onset or progression of neurodegenerative diseases; in addition, understanding the peculiar activity of this female hormone on inflammatory signalling pathways will possibly lead to the development of selected anti-inflammatory molecules. This review summarises the evidence for the involvement of microglia in neuroinflammation and the anti-inflammatory activity played by estrogens specifically in microglia.

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Estrogen and NGF synergistically protect terminally differentiated, ERα-transfected PC12 cells from apoptosis

Gollapudi

Oblinger

1999

J. Neurosci. Res.

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The potential cytoprotective effects of the gonadal steroid estrogen, acting via its receptor (ER) on target neurons, are of considerable interest in aging, disease, and trauma. In this study, we examined the effects of estrogen on a prototypical neuronal-like cell, namely, nerve growth factor (NGF) differentiated PC12 cells when these cells are placed into an apoptosis-inducing environment. A clonal line of PC12 cells stably transfected to express full-length rat ERalpha mRNA and protein (PCER cells), as well as control cells (vector DNA transfected: PCCON cells), were differentiated into neurite bearing cells by 14 days of NGF treatment. Reverse transcription polymerase chain reaction (RT-PCR) and immunocytochemistry for ERalpha revealed that terminally differentiated PCER cells continue to show robust ER mRNA and protein expression after differentiation. PCCON cells do not express ERalpha either before or after NGF-induced differentiation. After differentiation, serum and NGF withdrawal from wild type PC12 cells is well known to induce cell death via apoptotic mechanisms. We challenged differentiated PCER and PCCON cells with serum-free media and assessed the effects of various treatments on cell survival and apoptosis using trypan blue staining and quantitative TUNEL staining. When differentiated PCER cells were treated with 17beta-estradiol (E2) plus NGF during a 2-day serum-free media challenge, cell survival was significantly greater, and the apoptotic index was significantly lower, than when PCER cells were treated with NGF only during the challenge. No additional improvement in cell survival, and no further reduction in apoptosis, was observed in non-ER expressing cells (PCCON) by E2 plus NGF treatment over that obtained by NGF alone. The effects of E2 on the expression of several apoptosis-related genes in this system were also examined. We found that E2 treatment of differentiated PCER cells in serum-free media increased the levels of Bcl-XL mRNA and reduced the levels of BAD mRNA relative to those in vehicle-treated PCER cells, and also relative to those in PCCON cells. Thus, estrogen's protective effects on PCER cells appear to, at least partly, involve a modulation of apoptosis-regulating genes.

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Identification of Estrogen-Responsive Genes in Neuroblastoma SK-ER3 Cells

Cited by 64 publications

References 60 publications

Regulation of prothymosin α by estrogen receptor α: molecular mechanisms and relevance in estrogen-mediated breast cell growth

Regulation of prothymosin α by estrogen receptor α: molecular mechanisms and relevance in estrogen-mediated breast cell growth

Estrogen anti-inflammatory activity in brain: A therapeutic opportunity for menopause and neurodegenerative diseases

Estrogen and NGF synergistically protect terminally differentiated, ERα-transfected PC12 cells from apoptosis

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