Estrogen receptors colocalize with low-affinity nerve growth factor receptors in cholinergic neurons of the basal forebrain.

Toran-Allerand, C. Dominique; Miranda, Rajesh C.; Bentham, Wayne D. L.; Sohrabji, Farida; Brown, Theodore J.; Hochberg, Richard B.; MacLusky, Neil J.

doi:10.1073/pnas.89.10.4668

Cited by 395 publications

(153 citation statements)

References 47 publications

(47 reference statements)

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“…Thus, to further explore the mechanisms underlying ER-mediated protection of hearing, we evaluated the expression of the otoprotective agent BDNF protein in the cochlea of mice lacking ERβ and aromatase. Interactions between ERs and BDNF are apparent since an estrogen-sensitive response element has been identified in the BDNF gene (29,30).…”

Section: Introductionmentioning

confidence: 99%

Estrogen receptor β protects against acoustic trauma in mice

Meltser

Tahera

Simpson³

et al. 2008

J. Clin. Invest.

138

117

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The hormone estradiol affects the auditory system both by itself and by its interaction with neuroprotective factors. In this study, we examined the role of estrogen receptors (ERs) in response to auditory trauma. We found a ligand-dependent protective role for ERβ in the auditory system by investigating mice deficient in ERα (ERKO mice), ERβ (BERKO mice), and aromatase (ARKO mice). Basal auditory brainstem response (ABR) thresholds were similar in all animals. An acoustic trauma causing a temporary hearing loss raised ABR thresholds in male and female BERKO and ARKO mice compared with WT and ERKO mice. The ERα-selective agonist, propyl(1H) pyrazole-1,3,5-triyl-trisphenol (PPT), partially protected ARKO mice from trauma, while the ERβ-selective agonist, 2,3-bis (4-hydroxyphenyl)-propionitrile (DPN), protected WT and ARKO mice. Immunohistochemistry and western blotting confirmed the expression of ERβ in cochlea of WT males and females. Levels of brain-derived neurotrophic factor (BDNF), a neuroprotective peptide that can be induced by estrogen, was lower in BERKO and ARKO mice compared with WT. DPN treatment increased BDNF expression in ARKO mice. These data indicate ERβ-mediated neuroprotection involving BDNF in the auditory system of males and females.

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Section: Introductionmentioning

confidence: 99%

Estrogen receptor β protects against acoustic trauma in mice

Meltser

Tahera

Simpson³

et al. 2008

J. Clin. Invest.

138

117

View full text Add to dashboard Cite

show abstract

“…A large portion of BFCS neurons express E 2 receptors (ER), providing an anatomical substrate for actions of E 2 on this neurotransmitter system (Toran-Allerand et al, 1992;Mufson et al, 1999;Shughrue et al, 2000). It has been known for quite some time (Luine et al, 1975;McMillan et al, 1996) that E 2 modulates the cholinergic phenotype, but the specific cellular mechanisms remain unclear.…”

Section: Introductionmentioning

confidence: 99%

Morphological Effects of Estrogen on Cholinergic NeuronsIn VitroInvolves Activation of Extracellular Signal-Regulated Kinases

Dominguez¹,

Jalali²,

Lacalle³

2004

J. Neurosci.

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In the present study, we examined the ability of estrogen to enhance cholinergic neurite arborization in vitro and identified the signal transduction cascade associated with this effect. Basal forebrain primordia collected from rat pups on postnatal day 1 were cultured for 2 weeks and then treated with 5 nM 17␤-estradiol for 24 hr. Cholinergic neurons were identified immunocytochemically with an antibody against the vesicular acetylcholine transporter and digitally photographed. Morphological analysis indicated that female cultures respond to estrogen treatment with an increase in total neurite length per neuron (4.5-fold over untreated controls) and in total branch segment number per neuron (2.3-fold over controls). In contrast, there was no change in total neurite length per neuron in male cultures, and we also observed a decrease in total branch segment number per neuron (0.5-fold below controls). Detailed histograms indicated that estrogen increases primary and secondary branch length and number and also increases terminal neuritic branches to the seventh order in female cultures. In a second set of experiments, we investigated the signal transduction cascade involved in this response, and found that an upstream extracellular signal-regulated kinase (ERK) inhibitor blocked the ability of estrogen to enhance outgrowth in female cultures. Our study provides strong evidence in support of the fact that the ERK pathway is required for estrogen-induced structural plasticity in the cholinergic system of female rats. Understanding the intracellular processes that underlie the response of cholinergic neurons to estrogen provides a necessary step in elucidating how cholinergic neurons can be particularly susceptible to degeneration in postmenopausal women.

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“…[1][2][3][4][5][6][7][8][9] Among them, an involvement in carcinogenesis is of particular interest. [10][11][12] Consequently, the environmental effects of a synthetic estrogen, diethylstilbestrol (DES), large amounts of which have been used in stock-farming, have become a serious concern.…”

mentioning

confidence: 99%

Cytotoxicity of Synthetic Estrogen and Related Compounds in Various Tumor-Derived Cells.

Oda¹,

Tanaka

Sasaki

2001

Biological & Pharmaceutical Bulletin

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Various activities of estrogen, other than its primary activity as a hormone, have recently been revealed. [1][2][3][4][5][6][7][8][9] Among them, an involvement in carcinogenesis is of particular interest. [10][11][12] Consequently, the environmental effects of a synthetic estrogen, diethylstilbestrol (DES), large amounts of which have been used in stock-farming, have become a serious concern.We have shown that natural and synthetic estrogens and their related compounds have inhibitory activities on the in vitro polymerization of microtubule proteins, which play important roles in the cytoskeleton and cell division in addition to having hormonal activity. [13][14][15][16][17][18] We have also clarified that indenestrol A (IA), which is a metabolite of DES, has the highest antioxidant action among its related compounds. 19) Because the cytotoxicity of IA on colony formation by Chinese hamster V79 cells is similar to the effects of IA on microtubule proteins, the cytotoxicity is considered to be due partially to these effects on microtubule proteins. 16) We have also found that indenestrol B (IB), an isomer of IA, is highly cytotoxic to Chinese hamster V79 cells. 16) Taxol, which has the opposite effect of the well-known microtubule inhibitor colchicine, has drawn attention as a carcinostatic. However, the compounds related to synthetic estrogens mentioned in this study are more promising as carcinostatics, because their inhibitory activity against microtubule proteins is weaker than that of colchicine. In this study, cell growth inhibition by DES and its related compounds was examined by the MTT method using L1210, KB, and NIH-3T3 cells transformed with oncogenes, which are commonly used as screening systems for carcinostatics. MATERIALS AND METHODSMaterials DES and EE-dienestrol were obtained from Sigma Chemical Co. Other test compounds were synthesized as described previously. [12][13][14] Assay of in Vitro Antitumor Activity The assay of in vitro antitumor activity was performed using murine leukemia L1210 cells and human epidermoid carcinoma KB cells. NIH-3T3 cells transformed with oncogenes such as Ha-ras, Ki-ras, sis, abl, and src were obtained from the Virus Department of Kanazawa University. Roswell Park Memorial Institute medium 1640 supplemented with 10% heat-inactivated fetal bovine serum and kanamycin 50 mg/ml was used as the cell culture medium. The test compounds were dissolved in DMSO and added to the culture plates at 1% as the final volume. The DMSO concentration had no effect on the cytotoxicity. Tumor cells (2ϫ10 3 cells/ml) were cultured in 1 ml of the medium containing various concentrations of test compounds in a CO 2 gas incubator at 37°C for 72 h. Their viability, estimated by a modification of the colorimetric (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide) MTT assay, 20) was compared to that of control cells incubated in the same medium without the test compounds. The antitumor activity was evaluated as the IC 50 (the concentration [mM] of the compounds required for 50% ...

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Estrogen receptors colocalize with low-affinity nerve growth factor receptors in cholinergic neurons of the basal forebrain.

Cited by 395 publications

References 47 publications

Estrogen receptor β protects against acoustic trauma in mice

Estrogen receptor β protects against acoustic trauma in mice

Morphological Effects of Estrogen on Cholinergic NeuronsIn VitroInvolves Activation of Extracellular Signal-Regulated Kinases

Cytotoxicity of Synthetic Estrogen and Related Compounds in Various Tumor-Derived Cells.

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