estrogen receptor beta
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2022 ◽  
Vol 23 (2) ◽  
pp. 916
Author(s):  
Paulina Escandon ◽  
Sarah E. Nicholas ◽  
Rebecca L. Cunningham ◽  
David A. Murphy ◽  
Kamran M. Riaz ◽  
...  

Keratoconus (KC) is a progressive corneal thinning disease that manifests in puberty and worsens during pregnancy. KC onset and progression are attributed to diverse factors that include: environmental, genetics, and hormonal imbalances; however, the pathobiology remains elusive. This study aims to determine the role of corneal stroma sex hormone receptors in KC and their interplay with estrone (E1) and estriol (E3) using our established 3D in vitro model. Healthy cornea stromal cells (HCFs) and KC cornea stromal cells (HKCs), both male and female, were stimulated with various concentrations of E1 and E3. Significant changes were observed between cell types, as well as between males and females in the sex hormone receptors tested; androgen receptor (AR), progesterone receptor (PR), estrogen receptor alpha (ERα), and estrogen receptor beta (ERβ) using Western blot analysis. E1 and E3 stimulations in HCF females showed AR, PR, and ERβ were significantly upregulated compared to HCF males. In contrast, ERα and ERβ had significantly higher expression in HKC’s females than HKC’s males. Our data suggest that the human cornea is a sex-dependent, hormone-responsive tissue that is significantly influenced by E1 and E3. Therefore, it is plausible that E1, E3, and sex hormone receptors are involved in the KC pathobiology, warranting further investigation.


Author(s):  
Guitti Pourdowlat ◽  
Maryam Parvizi ◽  
Shogher Boyadjian ◽  
Masoud Shamaei ◽  
Mihan Pourabdollah

Background: Estrogen receptor beta (ERβ) is a potential target for cancer therapy as a tumor suppressor. Malignant pleural mesothelioma (MPM) is a rare but fatal cancer. This study tries to estimate the incidence of ERβ expression in the various subtypes of MPM tumors. Methods and Materials: In a retrospective study performed at a pulmonary tertiary referral hospital, formalin-fixed paraffin-embedded human tissues of 46 definitive MPM were evaluated for expression of ERβ by immunohistochemistry. Results: ERβ was detected in 14 cases (30.4%) out of the total 46 patients with a mean age of 58.08±11.59 SD, including 33 (71.7%) males. There was no statistically significant difference in patients with positive ERβ staining versus negative cases in age and sex (P >0.05). MPM subtypes included 36 (78.2%) cases of epithelioid mesothelioma, 3 (6.5%) cases of sarcomatoid, 5 (10.8%) cases of biphasic, and 2 (4.3%) cases of desmoplastic subtype. ERβ expression was observed only in epithelioid (11 of total 36 cases) and biphasic (3 of total 5 cases) tumors. There was no significant difference in the incidence of ERβ expression in different subtypes of malignant pleural mesothelioma. Statistical analysis shows a significant difference in the expression of ERβ in the epithelioid subtype (with a more favorable prognosis) versus non-epithelioid subtypes (with poor prognosis, including sarcomatoid, desmoplastic, and biphasic) (P = 0.024). Discussion and Conclusion: Considering the higher proportion of the epithelioid type of MPM with ERβ expression, this highlights the role of ERβ in target therapy of MPM tumor, especially in the epithelioid subtype with a more favorable prognosis. A better understanding of the pathology of mesothelioma will eventually contribute to the development of therapies beyond the existing therapeutic platform.


2022 ◽  
pp. 110246
Author(s):  
Rubí Hernández-Rojas ◽  
Carolina Jiménez-Arellano ◽  
Marisol de la Fuente-Granada ◽  
David Ordaz-Rosado ◽  
Rocío García-Becerra ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Stephanie A. Morris ◽  
Kenneth S. Korach ◽  
Katherine A. Burns

Endometriosis is a debilitating disease that affects about 10% of reproductive-aged adolescents and women. The etiology of the disease is unknown; however, a prevailing hypothesis is that endometriosis develops from retrograde menstruation, where endometrial tissue and fluids flow back through the oviducts into the peritoneal cavity. There is no cure for endometriosis, and symptoms are treated palliatively. Despite the advances in knowledge, the complexity of endometriosis etiology is still unknown. Recent work by our group suggests that the initiation of endometriosis is immune-dependent. Using a mouse model of endometriosis, we hypothesized the initiation of endometriosis is immune regulated and uterine endometrium specific. In the absence of a functional immune system non-obese diabetic/severe combined immunodeficiency (NOD/SCID mice), endometriotic lesions did not form. Uterine endometrial tissue forms endometriotic lesions, whereas tissues with differing basal expression levels of estrogen receptor alpha (ESR1) and estrogen receptor beta (ESR2), similar cellular composition to uterus (i.e. bladder, mammary gland, and lung), and treated with estradiol did not form lesions. As MMP7 is known to play a major role in the organization/reorganization of the endometrium during the menstrual cycle, blocking metalloproteinase (MMP) activity significantly decreased the invasive properties of these cells. Together, these findings suggest that endometriosis is immune and uterine specific and that MMP7 likely plays a role in the ability of uterine tissue and the innate immune system to establish and maintain endometriotic lesions.


Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3636
Author(s):  
Shuk-Mei Ho ◽  
Rahul Rao ◽  
Bin Ouyang ◽  
Neville N. C. Tam ◽  
Emma Schoch ◽  
...  

Gestational high butterfat (HFB) and/or endocrine disruptor exposure was previously found to disrupt spermatogenesis in adulthood. This study addresses the data gap in our knowledge regarding transgenerational transmission of the disruptive interaction between a high-fat diet and endocrine disruptor bisphenol A (BPA). F0 generation Sprague-Dawley rats were fed diets containing butterfat (10 kcal%) and high in butterfat (39 kcal%, HFB) with or without BPA (25 µg/kg body weight/day) during mating and pregnancy. Gestationally exposed F1-generation offspring from different litters were mated to produce F2 offspring, and similarly, F2-generation animals produced F3-generation offspring. One group of F3 male offspring was administered either testosterone plus estradiol-17β (T + E2) or sham via capsule implants from postnatal days 70 to 210. Another group was naturally aged to 18 months. Combination diets of HFB + BPA in F0 dams, but not single exposure to either, disrupted spermatogenesis in F3-generation adult males in both the T + E2-implanted group and the naturally aged group. CYP19A1 localization to the acrosome and estrogen receptor beta (ERbeta) localization to the nucleus were associated with impaired spermatogenesis. Finally, expression of methyl-CpG-binding domain-3 (MBD3) was consistently decreased in the HFB and HFB + BPA exposed F1 and F3 testes, suggesting an epigenetic component to this inheritance. However, the severe atrophy within testes present in F1 males was absent in F3 males. In conclusion, the HFB + BPA group demonstrated transgenerational inheritance of the impaired spermatogenesis phenotype, but severity was reduced in the F3 generation.


2021 ◽  
Author(s):  
Rhonda Voskuhl ◽  
Noriko Itoh ◽  
Cassandra Meyer ◽  
Yuichiro Itoh ◽  
Darian Mangu ◽  
...  

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.


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