Estrogen induces rapid translocation of estrogen receptor β, but not estrogen receptor α, to the neuronal plasma membrane

Sheldahl, Laird C; Shapiro, Robert A.; Bryant, Damani N.; Koerner, Ines P.; Dorsa, Daniel M.

doi:10.1016/j.neuroscience.2008.02.035

Cited by 67 publications

(58 citation statements)

References 79 publications

(104 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As previously reported (25)(26)(27), the classic hormonal mechanism involves the binding of estrogens to ERs in the nucleus, thus promoting the association with specific estrogen response elements in the promoters of target genes. At the same time, ERs regulate the expression of numerous genes without directly binding to DNA, but through protein-protein interactions with certain factors, such as phosphoinositide 3-kinase.…”

Section: Discussionmentioning

confidence: 78%

Cytoplasm estrogen receptor β5 as an improved prognostic factor in thymoma and thymic carcinoma progression

Wang

et al. 2015

Oncology Letters

View full text Add to dashboard Cite

Abstract. A number of previous studies have reported that sex steroid hormones, including estrogens, are involved in the regulation of the thymic function. The aim of the present study was to investigate the expression of estrogen receptor β5 (ERβ5) in thymic tumors and the correlation between ERβ5 expression and thymoma biological characteristics. The expression levels of ERβ5 in thymic epithelial tumors was evaluated in 103 patents using immunohistochemical staining and reverse transcription-quantitative polymerase chain reaction. In addition, an indirect immunofluorescence assay was performed to evaluate the ERβ5 expression levels in the TC1889 and T1682 cell lines. The survival outcome was estimated using Kaplan-Meier plots. The results indicated that ERβ5 expression was mainly located in the thymic tumor cell cytoplasm (87.37%; 90/103 cases) and overexpression was observed in thymic tumors compared with normal thymic tissues (P=0.001). Using the Kruskal-Wallis test, a statistically significant association was observed between cytoplasmic ERβ5 (cERβ5) expression and thymic tumor subtypes (P=0.024) and stages (P=0.003 and R=-0.376). The Kaplan-Meier plots revealed that cERβ5 expression was significantly associated with improved overall and progression-free survival (P=0.008 and P=0.004, respectively). The present study suggested that overexpression of cERβ5 may indicate an improved prognosis and may be involved in the underlying mechanism through which estrogen inhibits thymoma and thymic carcinoma development.

show abstract

Section: Discussionmentioning

confidence: 78%

Cytoplasm estrogen receptor β5 as an improved prognostic factor in thymoma and thymic carcinoma progression

Wang

et al. 2015

Oncology Letters

View full text Add to dashboard Cite

show abstract

“…Systemic E 2 treatment increases the distribution of ERb in dendritic spines and shafts in the adult female rat hippocampus (Waters et al 2011b), which may position ERb to interact with plasma membrane receptors in the dendrite to trigger cell signaling. In support of the notion that intracellular ERs act at the membrane are findings showing that E 2 causes ERb to translocate to the plasma membrane in hippocampal-derived cell lines and rat primary cortical neurons (Sheldahl et al 2008). At the membrane, ERa and ERb in neonatal female rats interact with metabotropic glutamate receptor 1 (mGluR1) to rapidly activate hippocampal extracellular signal-regulated kinase (ERK) signaling and promote phosphorylation of cAMP response element binding protein (CREB) (Boulware et al 2005.…”

Section: Estrogen Receptor Localization and Mechanism Of Action Era Amentioning

confidence: 97%

Sex steroid hormones matter for learning and memory: estrogenic regulation of hippocampal function in male and female rodents

et al. 2015

View full text Add to dashboard Cite

Ample evidence has demonstrated that sex steroid hormones, such as the potent estrogen 17b-estradiol (E 2 ), affect hippocampal morphology, plasticity, and memory in male and female rodents. Yet relatively few investigators who work with male subjects consider the effects of these hormones on learning and memory. This review describes the effects of E 2 on hippocampal spinogenesis, neurogenesis, physiology, and memory, with particular attention paid to the effects of E 2 in male rodents. The estrogen receptors, cell-signaling pathways, and epigenetic processes necessary for E 2 to enhance memory in female rodents are also discussed in detail. Finally, practical considerations for working with female rodents are described for those investigators thinking of adding females to their experimental designs.Hormones have long been known to play key roles in regulating learning and memory. Many hormones, including epinephrine, glucocorticoids, and insulin influence learning and memory via inverted U-shaped dose-response relationships in which memory is enhanced by moderate, but not low or high, hormone levels (Roozendaal 2000;Korol and Gold 2007;McNay and Recknagel 2011). Research from the past two decades has demonstrated that sex steroid hormones, particularly the potent estrogen 17b-estradiol (E 2 ), also regulate learning and memory in male and female rodents via an inverted U-shaped dose-response function that is influenced by estrogen receptor expression (Packard and Teather 1997a;Packard 1998;Foster 2012). Yet E 2 has not gained widespread acceptance as a hormonal modulator of memory in both females and males, perhaps because the majority of this research has been conducted in female rodents. Moreover, the common view of E 2 as a "female" hormone may contribute to the misperception that E 2 is not relevant for cognitive function in males. However, considerable evidence supports a vital role for E 2 in mediating neural function and behavior in male rodents. Therefore, it is important for investigators working with males to understand the ways in which E 2 and other sex steroid hormones (e.g., androgens, progestins, and other estrogens) may influence their brain regions and behaviors of interest.Another reason for investigators to be cognizant of sex steroid hormone-induced regulation of learning and memory is that males and females may respond differently to various treatments and environmental factors. A classic example is that of acute stress, which enhances classical conditioning and increases apical CA1 dendritic spine density in male rats, but impairs classical conditioning and decreases CA1 spine density in female rats (Wood and Shors 1998;Shors et al. 2001). Therefore, investigators hoping to comply with National Institutes of Health policies that encourage the inclusion of females in biomedical research must be aware that adding females to a study is not as simple as adding another group. In some ways, females are fundamentally different from males, the most obvious of which is the presence of reproductive...

show abstract

“…Immunohistochemical techniques have visualized membrane ERα in a variety of cell types including endometrial and breast cancer cells [103], pituitary cells [104], and lung cancer cells/tumors [91]. ERβ was shown to be located in the PM of primary cortical neurons in recent confocal imaging studies [105]. Overall, the PM localization of ER appears to be cell type-specific.…”

Section: Introductionmentioning

confidence: 99%

Estrogen Regulation of MicroRNA Expression

Klinge

2009

136

110

View full text Add to dashboard Cite

Women outlive men, but life expectancy is not influenced by hormone replacement (estrogen + progestin) therapy. Estrogens appear to protect brain, cardiovascular tissues, and bone from aging. Estrogens regulate genes directly through binding to estrogen receptors alpha and beta (ERα and ERβ) that are ligand-activated transcription factors and indirectly by activating plasma membrane-associated ER which, in turns, activates intracellular signaling cascades leading to altered gene expression. MicroRNAs (miRNAs) are short (19-25 nucleotides), naturally-occurring, non-coding RNA molecules that base-pair with the 3’ untranslated region of target mRNAs. This interaction either blocks translation of the mRNA or targets the mRNA transcript to be degraded. The human genome contains ~ 700-1,200 miRNAs. Aberrant patterns of miRNA expression are implicated in human diseases including breast cancer. Recent studies have identified miRNAs regulated by estrogens in human breast cancer cells, human endometrial stromal and myometrial smooth muscle cells, rat mammary gland, and mouse uterus. The decline of estradiol levels in postmenopausal women has been implicated in various age-associated disorders. The role of estrogen-regulated miRNA expression, the target genes of these miRNAs, and the role of miRNAs in aging has yet to be explored.

show abstract

Estrogen induces rapid translocation of estrogen receptor β, but not estrogen receptor α, to the neuronal plasma membrane

Cited by 67 publications

References 79 publications

Cytoplasm estrogen receptor β5 as an improved prognostic factor in thymoma and thymic carcinoma progression

Cytoplasm estrogen receptor β5 as an improved prognostic factor in thymoma and thymic carcinoma progression

Sex steroid hormones matter for learning and memory: estrogenic regulation of hippocampal function in male and female rodents

Estrogen Regulation of MicroRNA Expression

Contact Info

Product

Resources

About