scholarly journals Mind the Gap: Estrogen receptor beta (ERβ) in astrocytes is a therapeutic target to prevent cognitive problems at menopause.

2021 ◽  
Author(s):  
Rhonda Voskuhl ◽  
Noriko Itoh ◽  
Cassandra Meyer ◽  
Yuichiro Itoh ◽  
Darian Mangu ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Cognitive Deficits ◽  
Therapeutic Target ◽  
Brain Aging ◽  
Hormone Replacement ◽  
Unmet Need ◽  
Estrogen Receptor Beta ◽  
Cognitive Testing ◽  
Specific Cell ◽  
Receptor Beta

Abstract Aging is a risk factor for cognitive decline and susceptibility to neurodegenerative diseases. Some aspects of aging, like the loss of sex hormones, may be preventable. Menopause is associated with cognitive deficits and brain atrophy. Since standard hormone replacement therapy (HRT) does not mitigate these brain aging outcomes, a gap in knowledge involves understanding brain region-specific, cell-specific, and receptor-specific mechanisms underlying this neurodegeneration. Here, cognitive testing and in vivo magnetic resonance imaging demonstrated that ovarian hormones in female mice at midlife protect against hippocampal-dependent cognitive impairment and dorsal hippocampal atrophy. Further, this neuroprotection in females at midlife is lost in mice with selective deletion of estrogen receptor beta (ERβ) in astrocytes, but not neurons. This preclinical evidence identifies ERβ in astrocytes as a novel therapeutic target to prevent hippocampal-dependent cognitive deficits and reduce posterior hippocampus atrophy in menopausal women, a major unmet need in half the population.

Distribution of estrogen receptor beta (ERβ) mRNA in hypothalamus, midbrain and temporal lobe of spayed macaque: continued expression with hormone replacement

2000 ◽  
Vol 76 (2) ◽  
pp. 191-204 ◽  
Author(s):  
Chrisana Gundlah ◽  
Steven G Kohama ◽  
Stephanie J Mirkes ◽  
Vasilios T Garyfallou ◽  
Henryk F Urbanski ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Temporal Lobe ◽  
Hormone Replacement ◽  
Estrogen Receptor Beta ◽  
Receptor Beta

Abstract 1858: Estrogen receptor beta as a tractable therapeutic target

2015 ◽  
Author(s):  
Carly S. Filgueira ◽  
Cindy Benod ◽  
Xiaohua Lou ◽  
Anders Strom ◽  
Jan-Åke Gustafsson ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Therapeutic Target ◽  
Estrogen Receptor Beta ◽  
Receptor Beta

scholarly journals Estradiol and progesterone regulate proliferation and apoptosis in colon cancer

2019 ◽  
Vol 8 (3) ◽  
pp. 217-229 ◽  
Author(s):  
Corina Verónica Sasso ◽  
Flavia Eliana Santiano ◽  
Fiorella Campo Verde Arboccó ◽  
Leila Ester Zyla ◽  
Silvana Noemí Semino ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Estrogen Receptor ◽  
Hormonal Regulation ◽  
Hormone Replacement ◽  
Combined Treatment ◽  
Estrogen Receptor Beta ◽  
Ovariectomized Rats ◽  
Colon Tumors ◽  
Proliferation And Apoptosis ◽  
Receptor Beta

Epidemiological studies describe estrogens as protectors in the development of colon cancer in postmenopausal women treated with hormone replacement therapy. However, the role of progesterone in colon cancer has been minimally studied and the results are controversial. For the above, the objective of this work was to determine the hormonal regulation exerted by natural ovarian steroids on proliferation and apoptosis in an experimental model of colon cancer in ovariectomized rats treated with 17-beta estradiol and progesterone. Sprague–Dawley rats were exposed to the carcinogen 1,2-dimethylhydrazine to induce colon tumors. Thirty days later, the rats were ovariectomized and treated with estradiol (60 μg/kg), progesterone (10 mg/kg), estradiol plus progesterone (60 μg/kg and 10 mg/kg) or vehicle. We observed no significant differences in colon cancer incidence and tumor multiplicity between the groups. Nevertheless, we observed a decrease in PCNA expression and a greater number of apoptotic index, higher expression of caspase 3, cleaved PARP and cleaved caspase 8 in tumors, confirming the activation of the extrinsic pathway of apoptosis by the combined treatment. In addition, we observed a higher expression of estrogen receptor beta in these tumors. We conclude that the action of both hormones, estradiol and progesterone, is necessary to reduce proliferation and increase apoptosis in colon tumors, probably through estrogen receptor beta activation.

Assessment of Estrogen Receptor Beta in Patients with Triple Negative Breast Cancer

2020 ◽  
Vol 106 (1_suppl) ◽  
pp. 38-38
Author(s):  
HS Mubisi ◽  
MM Farouk ◽  
II Zaki ◽  
TA El Fayoiem ◽  
AA Ismail
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Lymph Nodes ◽  
Triple Negative Breast Cancer ◽  
Tumor Size ◽  
Therapeutic Target ◽  
Triple Negative ◽  
Estrogen Receptor Beta ◽  
Ki 67 ◽  
Receptor Beta

Introduction: Triple negative breast cancer (TNBC), defined as lacking the expression of estrogen receptor alpha (ERα), progesterone receptor and human epidermal growth factor receptor is an aggressive breast cancer subtype for which there is a need to identify new therapeutic targets. About 50-80% of TNBC express Estrogen Receptor Beta (ERβ). Given its slight differences from ERα in terms of structure, signaling and its anti-proliferative effects on breast cancer cells, ERβ may be a possible therapeutic target. This study sought to assess the presence of ERβ and its correlation with the clinico-pathological features among the Egyptian females with TNBC. Material and Methods: The study was a retrospective analysis. The following data was retrieved from patient’s files and recorded: age, tumor size, lymph nodes metastasis, and stage. Paraffin blocks for patients confirmed by IHC to be TNBC were subjected to immunohistochemical staining for ERβ, CK5/6, and Ki 67. Results: ERβ was positive in 80% of cases (n=32/40). ERβ significantly correlated with Age (rs = -0.473, P = 0.002, n = 40), Tumor size (rs = -0.471, P = 0.007, n = 40), Lymph nodes (rs = -0.365, P = 0.021, n =40), and Stage (rs = -0.468, P = 0.002, n = 40). There was no correlation between ERβ with Ki-67 and CK5/6 a marker of the basal phenotype. All 8 patients without ERβ had an aggressive disease. 4 received neoadjuvant chemotherapy with minimum or no pathologic complete response in the axillary lymph nodes, 2 presented with upfront metastatic disease while the other 2 were cases of local recurrence with a change in the molecular phenotype of the tumor from luminal subtype to TNBC. Conclusion: This study shows ERβ expression occurs in TNBC. It may have the potential to become a therapeutic target for TNBC.

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