scholarly journals Unique Sensitivity of Uterine Tissue and the Immune System for Endometriotic Lesion Formation

2021 ◽  
Vol 12 ◽  
Author(s):  
Stephanie A. Morris ◽  
Kenneth S. Korach ◽  
Katherine A. Burns
Keyword(s):  
Estrogen Receptor ◽  
Immune System ◽  
Estrogen Receptor Alpha ◽  
Severe Combined Immunodeficiency ◽  
Estrogen Receptor Beta ◽  
Endometrial Tissue ◽  
Uterine Tissue ◽  
Retrograde Menstruation ◽  
Uterine Endometrium ◽  
Basal Expression

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.

scholarly journals Calcium and Phosphorus Levels in Saliva are Influenced by Genetic Polymorphisms in Estrogen Receptor Alpha and Microrna17

2020 ◽  
Vol 31 (5) ◽  
pp. 466-470
Author(s):  
Erika Calvano Küchler ◽  
Raquel Fernanda Gerlach ◽  
Arthur S Cunha ◽  
Lucas A Ramazzotto ◽  
Paula Porto Spada ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Genetic Polymorphisms ◽  
Estrogen Receptor Alpha ◽  
Estrogen Receptor Beta ◽  
Chi Square ◽  
Receptor Alpha ◽  
High Calcium ◽  
Calcium And Phosphorus ◽  
Receptor Beta ◽  
Phosphorus Levels

Abstract Homeostasis between salivary calcium and phosphorus is important for maintaining oral health. The aim of this study was to evaluate if polymorphisms in ESR1 (Estrogen Receptor Alpha), ESR2 (Estrogen Receptor Beta) and miRNA17 (microRNA17) are associated with calcium and phosphorus levels in saliva. Saliva from 276 12-year-old children were collected by masticatory stimulation and calcium and phosphorus levels were determined by Mass Spectrometry. Genomic DNA was extracted from remaining saliva and genetic polymorphisms in ESR1 (rs12154178, rs1884051, rs9340799 and rs2234693), in ESR2 (rs4986938 and rs1256049) and in miRNA17 (rs4284505) were genotyped using TaqMan chemistry and a real-time PCR equipment. Statistical differences in genotype and allele distributions between ‘low’ and ‘high’ calcium and phosphorus levels were determined using chi-square or Fisher´s exact tests. The analysis was also adjusted by sex (alpha of 5%). ESR1 rs9340799 had the less common genotype associated with higher calcium levels (p=0.03). The less common allele of ESR1 rs1884051 was associated with lower phosphorus levels (p=0.005) and there was an excess of heterozygotes for miRNA17 rs4284505 among individuals with lower calcium levels (p=0.002), both adjusted by sex. This study provides evidence that genetic polymorphisms in ESR1 and miRNA17 are involved in determining salivary calcium and phosphorus levels.

Abstract P130: Estrogen Receptor β Mediates the Rescue of Cardiac Function in Advanced Heart Failure by Promoting Neoangiogenesis and Reducing Fibrosis

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Andrea Iorga ◽  
Rod Partow-Navid ◽  
Humann Matori ◽  
Jingyuan Li ◽  
Soban Umar ◽  
...  
Keyword(s):  
Heart Failure ◽  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Cardiac Fibrosis ◽  
Biological Effects ◽  
Estrogen Receptor Beta ◽  
Pressure Overload ◽  
Decompensated Heart Failure ◽  
Beta Agonist ◽  
Receptor Beta

Estrogen can act via the estrogen receptor alpha (ERa) or estrogen receptor beta (ERb) to exert its biological effects, and both of these receptors are present in the heart. We have previously shown that short-term estrogen (E2) treatment can rescue pressure overload-induced decompensated heart failure (HF) in mice, and that this rescue is achieved mainly through the ERb. Furthermore, E2 has been shown to regulate angiogenesis in different tissues. Because HF has been associated with decreased angiogenesis and increased fibrosis, here we investigated whether the E2-induced rescue of HF by the selective ERb agonist DPN can regulate cardiac fibrosis and neoangiogenesis. We used transaortic constriction to induce HF, and once the ejection fraction (EF) reached ∼30%, one group of animals was sacrificed (HF group), and the other three groups received either 17b-estradiol via a subcutaneous pellet implant (0.012mg/pellet, n=16), selective ERa agonist (PPT, 0.625mg/kg/day), or selective ERb agonist (DPN, 0.625mg/kg/day) for 10 days. Serial echocardiography was performed to monitor cardiac structure and function. As expected, E2 rescued HF by restoring EF from 33.17±1.12% to 53.05±1.29%. Mice treated with DPN had a significant EF improvement from 33.17±1.12% to 45.25±2.1% (n=7), while the EF of PPT-treated mice did not improve (31.09±2.3%, n=6). Similarly, only the fractional shortening of DPN-treated mice improved from 15.7±0.58% in HF to 21.95±1.65% with DPN treatment vs. 14.72±1.24% with PPT. Next, we examined whether promotion of cardiac neoangiogenesis and suppression of fibrosis by the selective ERb agonist are possible mechanisms in the rescue action of HF by DPN. DPN treatment was able to reverse the interstitial and perivascular fibrosis observed in HF, while PPT had no effect. The selective ERb agonist also stimulated neoangiogenesis, as the capillary density was increased from 0.46±0.04 microvessels/cardiomyocyte in HF to 0.67±0.07 with DPN treatment, whereas PPT treatment had no effect (0.43±0.03). Our data strongly suggests that upregulation of cardiac neoangiogenesis and reversal of fibrosis are pivotal mechanisms in rescuing advanced HF by the estrogen receptor beta agonist DPN.

Assessment of the Levels of ER and PR v1

2021 ◽  
Author(s):  
Dhimas Hari Sakti
Keyword(s):  
Polymerase Chain Reaction ◽  
Estrogen Receptor ◽  
Real Time ◽  
Estrogen Receptor Alpha ◽  
Estrogen Receptor Beta ◽  
Chain Reaction ◽  
Receptor Alpha ◽  
Polymerase Chain ◽  
Receptor Beta

Measuring the level of estrogen receptor alpha, estrogen receptor beta, and progesteron receptor in meningioma tissue using quantitative real-time polymerase chain reaction.

scholarly journals An Immunohistochemical Study on the Expression of Sex Steroid Receptors in Canine Mammary Tumors

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Leena Rajathy Port Louis ◽  
Khub Chandra Varshney ◽  
Madhavan Gopalakrishnan Nair
Keyword(s):  
Estrogen Receptor ◽  
Epithelial Cells ◽  
Estrogen Receptor Alpha ◽  
Malignant Tumors ◽  
Steroid Receptors ◽  
Estrogen Receptor Beta ◽  
Smooth Muscles ◽  
Mammary Tumors ◽  
Benign Tumors ◽  
Canine Mammary Tumors

Steroid hormones are found to play a major role in the genesis and progression of mammary tumors. The aim of this study was to immunohistochemically detect the presence of estrogen receptor alpha (ERα), estrogen receptor beta (ERβ), and progesterone receptor (PR) and also to study the association between these markers in 29 cases of benign (11) and malignant (18) canine mammary tumors. ERα immunostaining was noticed in only one case of carcinosarcoma specifically in the nuclei of epithelial and a few myoepithelial cells. ERβ immunostaining was noticed in the nuclei and cytoplasm of epithelial cells and smooth muscles lining the blood vessels. Immunoexpression of ERβ was 82% in benign tumors and 78% in malignant tumors. PR immunostaining was expressed in the nuclei of epithelial cells in both benign and malignant tumors. Among the 15 PR+ cases, 6 (55%) were of benign type, and 9 (50%) were of malignant type. The most common group of hormone receptor was the ERα−/PR+/ERβ+ (46%) in benign tumors and ERα−/PR−/ERβ+ (38%) in malignant tumors. Although there was no significant association between ERα and PR with ERβ, the findings indicated that ERβ was consistently expressed in both benign and malignant tumors, irrespective of ERα and PR status.

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