Estrogen Receptor Is Expressed in Different Types of Glial Cells in Culture

Santagati, Sabrina; Melcangi, Roberto Cosimo; Celotti, F.; Martini, L.; Maggi, Adriana

doi:10.1046/j.1471-4159.1994.63062058.x

Cited by 147 publications

(74 citation statements)

References 13 publications

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“…This cell type has the greatest potential for a critical role in steroid-mediated protection of neurons in the brain, since ablation of astrocytes in vivo results in a significant decrease in neuronal survival (Cui et al 2001). Indeed, astrocytes are well-described target cells for E and P expressing the corresponding nuclear steroid receptors (Jung Testas et al 1992, Santagati et al 1994, Beyer 1999, Quadros et al 2007. Confirming previously published data (Pawlak et al 2005), we observed transcripts for ERa, ERb, and PR in cortical astrocytes from both genders.…”

Section: Discussionsupporting

confidence: 88%

Gender-specific regulation of mitochondrial fusion and fission gene transcription and viability of cortical astrocytes by steroid hormones

Arnold¹,

Araújo²,

Beyer³

2008

Journal of Molecular Endocrinology

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Astroglia and steroid hormones such as estrogen and progesterone regulate cell growth, function, and protection in the central nervous system (CNS). It appears that astrocytes and steroids act in concert to promote cell survival under pathological conditions. With respect to the role of mitochondrial fusion and fission in energy metabolism, apoptosis, and proliferation, astrocyte mitochondria resemble a perfect intracellular target for steroids to modulate these processes, thereby promoting cell vitality after damage. We have studied the effects of estrogen and progesterone on cell viability in comparison with mitochondrial fusion and fission gene transcription in primary cortical astrocytes from female and male mouse brains. Estrogen-and progesterone-treated female astrocytes demonstrated an increase in cell number and proliferation marker accompanied by an upregulation of fusion and fission gene transcription, which were apparently balancing pro-and anti-apoptotic processes. On the other hand, male astrocytes exhibited no change in cell number after estrogen treatment, but a decrease after progesterone administration. This could be the consequence of stimulated apoptosis in male astrocytes by both steroids, which was counterbalanced by an increased proliferation in the presence of estrogen, whereas it was strengthened in the presence of progesterone. Supportively, estrogen promoted and progesterone decreased the transcription of fusion and fission genes. We suggest that estrogen and progesterone affect mitochondrial fusion and fission gene transcription in cortical astrocytes in a gender-specific way, thereby influencing mitochondrial function differently in both genders. Thus, interaction of sex steroids with mitochondria may represent one possible cause for gender differences in cellular pathology in the CNS.

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Section: Discussionsupporting

confidence: 88%

Gender-specific regulation of mitochondrial fusion and fission gene transcription and viability of cortical astrocytes by steroid hormones

Arnold¹,

Araújo²,

Beyer³

2008

Journal of Molecular Endocrinology

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“…Oestrogen receptors present in primary glial cell cultures and different types of glial cells (Jung-Testas et al, 1992;Santagati et al, 1994;Yague et al, 2004) allow this non-neuronal cells of the CNS to respond to oestrogens; so glioma cells were able to respond significantly to oestradiol in the culture. Melatonin, only at 1 mM concentration, counteracted the growth stimulatory effect of oestradiol on C6 cells.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effects of pharmacological doses of melatonin on aromatase activity and expression in rat glioma cells

et al. 2007

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Melatonin exerts oncostatic effects on different kinds of neoplasias, especially on oestrogen-dependent tumours. Recently, it has been described that melatonin, on the basis of its antioxidant properties, inhibits the growth of glioma cells. Glioma cells express oestrogen receptors and have the ability to synthesise oestrogens from androgens. In the present study, we demonstrate that pharmacological concentrations of melatonin decreases the growth of C6 glioma cells and reduces the local biosynthesis of oestrogens, through the inhibition of aromatase, the enzyme that catalyses the conversion of androgens into oestrogens. These results are supported by three types of evidence. Firstly, melatonin counteracts the growth stimulatory effects of testosterone on glioma cells, which is dependent on the local synthesis of oestrogens from testosterone. Secondly, we found that melatonin reduces the aromatase activity of C6 cells, measured by the tritiated water release assay. Finally, by (RT) -PCR, we found that melatonin downregulates aromatase mRNA steady-state levels in these glioma cells. We conclude that melatonin inhibits the local production of oestrogens decreasing aromatase activity and expression. By analogy to the implications of aromatase in other forms of oestrogen-sensitive tumours, it is conceivable that the modulation of the aromatase by pharmacological melatonin may play a role in the growth of glioblastomas.

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“…E 2 alters many aspects of hippocampal morphology, including synapse number, spine density, and astrocytic volume (50)(51)(52). In brain, astrocytes contain ER␤ (53,54). Moreover, ER␤KO brains display fewer Nissl-stained neurons and increased glial fibrillary acidic protein immunoreactive cells in the medial amygdala and preoptic area, as compared with WT littermates (55).…”

Section: Discussionmentioning

confidence: 99%

Disruption of estrogen receptor β gene impairs spatial learning in female mice

Rissman

Heck

Leonard

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

225

136

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Here we provide the first evidence, to our knowledge, that estradiol (E 2) affects learning and memory via the newly discovered estrogen receptor ␤ (ER␤). In this study, ER␤ knockout (ER␤KO) and wild-type littermates were tested for spatial learning in the Morris water maze after ovariectomy, appropriate control treatment, or one of two physiological doses of E 2. Regardless of treatment, all wild-type females displayed significant learning. However, ER␤KOs given the low dose of E 2 were delayed in learning acquisition, and ER␤KOs administered the higher dose of E2 failed to learn the task. These data show that ER␤ is required for optimal spatial learning and may have implications for hormone replacement therapy in women.T he steroid hormone estradiol (E 2 ) either is required for or significantly modulates many behaviors, including cognitive behaviors (1-9). Learning tasks that involve reference memory tend to be impaired by E 2 (1,7,8). In contrast, low levels of E 2 may facilitate working memory (5, 9). In women, changes in ability on visuospatial tasks and memory recall over the menstrual cycle have been documented (10, 11). Also, beneficial effects of estrogen replacement on cognition have been noted in normally aging women (12, 13) and in women suffering from dementia associated with Alzheimer's disease (14,15).How estrogen acts on learning and memory is not clear. Estrogen binding has been reported throughout the rodent brain, including the hippocampus and cortex (16). Both characterized nuclear estrogen receptors (ER␣ and -␤) are present in extrahypothalamic regions (17,18). In addition, in vitro work suggests that estrogen acts in a nongenomic fashion in hippocampal tissues (19,20). Mice lacking functional ER␣ have severe deficits in several aspects of reproduction, including behavior (21-24). On the other hand, ER␤ knockout mice (ER␤KO) are subfertile, and sexual behavior is normal (25, 26). Thus, there has been speculation that ER␤ regulates estrogen's nonreproductive functions in the central nervous system (21, 27, 28).Here we describe our work on spatial learning in female ER␤KO mice. When treated with doses of E 2 that do not affect learning in wild-type (WT) littermates, ER␤KO mice had impaired ability to escape from the Morris water maze. Interactions between ER␣ and -␤ may contribute to the learning response; to test the hypothesis that lack of ER␤ influences the level of ER␣ protein, mouse brains were examined for ER␣ immunoreactivity (ER␣-ir), with emphasis on the hippocampus (HIPP). MethodsAnimals. Female mice (ages 5-7 mos) were of mixed 129͞J and C57BL͞6J background. Subjects were generated by crossing heterozygotic mating pairs carrying a single copy of the disrupted ER␤ gene (25). The resulting offspring were genotyped by PCR amplification of tail DNA. WT and ER␤ disrupted (ER␤KO) littermates were used in these studies. The ER␤ gene disruption was created by Neo insertion into exon 3 (25), thus the following three primers were used: one from intron 2 (5Ј-GGAGTAGAAACAAGCAATCCAGACATC-3Ј), a...

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Estrogen Receptor Is Expressed in Different Types of Glial Cells in Culture

Cited by 147 publications

References 13 publications

Gender-specific regulation of mitochondrial fusion and fission gene transcription and viability of cortical astrocytes by steroid hormones

Gender-specific regulation of mitochondrial fusion and fission gene transcription and viability of cortical astrocytes by steroid hormones

Inhibitory effects of pharmacological doses of melatonin on aromatase activity and expression in rat glioma cells

Disruption of estrogen receptor β gene impairs spatial learning in female mice

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