ISDN2014_0191: REMOVED: Protective role of 17β‐estradiol on glucose transporter and mitochondrial enzymes in brain of aging female rats

2015 ◽  
Vol 47 (Part_A) ◽  
pp. 56-56
Author(s):  
Pardeep Kumar ◽  
R.K. Kale ◽  
N.Z. Baquer
Keyword(s):  
Glucose Transporter ◽  
Protective Role ◽  
Female Rats ◽  
Mitochondrial Enzymes ◽  
17Β Estradiol

scholarly journals Protective role of 17β-estradiol treatment in renal injury on female rats submitted to brain death

2021 ◽  
Vol 0 (0) ◽  
pp. 0-0
Author(s):  
Roberto Armstrong-Jr ◽  
Fernanda Yamamoto Ricardo-da-Silva ◽  
Marina Vidal-dos-Santos ◽  
Cristiano de Jesus Correia ◽  
Lucas Ferreira Anunciação ◽  
...  
Keyword(s):  
Brain Death ◽  
Renal Injury ◽  
Protective Role ◽  
Female Rats ◽  
Estradiol Treatment ◽  
17Β Estradiol

Abstract 237: Sex-specific Regulation Of Collagen I And III Expression By 17β-estradiol In Rat Cardiac Fibroblasts: Role Of Estrogen Receptors

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Elke Dworatzek ◽  
Shokoufeh Mahmoodzadeh ◽  
Sandra Kunze ◽  
Vera Regitz-Zagrosek
Keyword(s):  
Sex Differences ◽  
Western Blot ◽  
Estrogen Receptors ◽  
Cardiac Fibrosis ◽  
Cardiac Fibroblasts ◽  
Collagen I ◽  
Female Rats ◽  
17Β Estradiol ◽  
Specific Regulation

Clinical and animal studies showed in female pressure-overloaded hearts less cardiac fibrosis and collagen I and III gene expression compared to males, suggesting an inhibitory effect of 17β-Estradiol (E2) on collagens. Therefore we investigated the role of E2 and estrogen receptors (ER) on collagen I and III expression in isolated rat cardiac fibroblasts from both sexes. Cardiac fibroblasts were isolated from adult male and female Wistar rats, and treated with E2 (10-8M), vehicle, ERα and ERβ-agonist (10-7M) and/or pre-treated with ICI 182,780 (10-5M) for 24h. Cellular localization of ER in cardiac fibroblasts with/without E2 was detected by immunofluorescence staining, and expression of both ER was determined by western blot. Expression of collagen I and III was determined by qRT-PCR and western blot. E2-treatment led to a nuclear translocation of ERα and ERβ in cardiac fibroblasts, suggesting the functional activity of ER as transcription factors. Furthermore in cardiac fibroblasts from female rats E2 led to a significant down-regulation of collagen I and III gene and protein expression. In contrast there was a significant increase of collagen I and III levels in fibroblasts isolated from male rat hearts by E2. E2-effect could be inhibited by ICI 182, 780 indicating the involvement of ER. In cardiac fibroblasts from female rats, ERα-agonist treatment led to a significant down-regulation of collagen I and III mRNA level, but ERβ-agonist had no effects. In contrast, ERβ-agonist treatment of cardiac fibroblasts from males increased collagen I and III mRNA, but no changes with ERα agonist-treatment were detected. ERα protein levels displayed no sex differences at basal level. After E2-treatment ERα protein was up-regulated in male cells, but decreased in cardiac fibroblasts from females. ERβ protein was higher in female cells compared to males, but the expression was not regulated by E2 in both sexes. Sex-specific regulation of collagen I and III expression by E2 in cardiac fibroblasts might be responsible for sex-differences in cardiac fibrosis. This might be due to sexually dimorphic ER expression and regulation. Understanding how E2 and ER mediate sex-differences in cardiac remodeling may help to design sex-specific pharmacological interventions.

scholarly journals The Effect of a Mediterranean Meal on Sprague Dawley Rats DMBA-Induced Mammary Tumors

2010 ◽  
Vol 3 ◽  
pp. CGM.S5894
Author(s):  
Paula C. Pereira ◽  
A. Filipa Vicente ◽  
Maria F. Mesquita ◽  
Antonio S. Cabrita
Keyword(s):  
Experimental Studies ◽  
Protective Role ◽  
Female Rats ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Total Cancer ◽  
Group A ◽  
Histopathologic Analysis ◽  
Group B

The present study intents to find a possible protective role of a Mediterranean type meal on mammary carcinogenesis. Several factors have been associated with breast cancer risk, genetics and environment are the most pointed out in epidemiologic and experimental studies. Diet is an environmental factor that can promote or prevent disease, being responsible for almost 35% of total cancer cases. A total of 72 female rats 50 days old were randomly divided in three groups of 24 rats and housed 4 in each plastic cage in a holding room under constant conditions of 22 ± 2 °C, 55 ± 10% humidity and a 12 h light/dark cycle. All the animals were submitted to the administration of 20 mg of 7, 12 dimethylbenzanthracene (DMBA) in olive oil, by gavages, except group A. The same defined standard food was provided for all the animals in group A and B, supplemented with a Mediterranean meal in group C. All the animals were sacrificed by the end of 150 days. Total carcinoma number did not differ significantly between Groups B and C and there were not found any neoplastic lesions in Group A. Most tumors showed a mixed architectural pattern, with cribriform and papillary areas, comedocarcinoma and necrosis was only seen in Group B. Histopathologic analysis showed that Group C tumors had lower mitotic activity and Pattern Grades, but higher Nuclear Grades. Mediterranean diet type meal showed lower Pattern Grades and lower Mitotic count in spite of that a higher nuclear pleomorphism was also found. Even so, tumors from Group C were better differentiated which can indicate lower malignancy.

scholarly journals 17β-estradiol improves hepatic mitochondrial biogenesis and function through PGC1B

2017 ◽  
Vol 232 (2) ◽  
pp. 297-308 ◽  
Author(s):  
Bel M Galmés-Pascual ◽  
Antonia Nadal-Casellas ◽  
Marco Bauza-Thorbrügge ◽  
Miquel Sbert-Roig ◽  
Francisco J García-Palmer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Biogenesis ◽  
Oxidative Capacity ◽  
Protective Role ◽  
Rat Tissues ◽  
Peroxisome Proliferator ◽  
Ovx Rats ◽  
17Β Estradiol ◽  
And Function

Sexual dimorphism in mitochondrial biogenesis and function has been described in many rat tissues, with females showing larger and more functional mitochondria. The family of the peroxisome proliferator-activated receptor gamma coactivator 1 (PGC1) plays a central role in the regulatory network governing mitochondrial biogenesis and function, but little is known about the different contribution of hepatic PGC1A and PGC1B in these processes. The aim of this study was to elucidate the role of 17β-estradiol (E2) in mitochondrial biogenesis and function in liver and assess the contribution of both hepatic PGC1A and PGC1B as mediators of these effects. In ovariectomized (OVX) rats (half of which were treated with E2) estrogen deficiency led to impaired mitochondrial biogenesis and function, increased oxidative stress, and defective lipid metabolism, but was counteracted by E2 treatment. In HepG2 hepatocytes, the role of E2 in enhancing mitochondrial biogenesis and function was confirmed. These effects were unaffected by the knockdown of PGC1A, but were impaired when PGC1B expression was knocked down by specific siRNA. Our results reveal a widespread protective role of E2 in hepatocytes, which is explained by enhanced mitochondrial content and oxidative capacity, lower hepatic lipid accumulation, and a reduction of oxidative stress. We also suggest a novel hepatic protective role of PGC1B as a modulator of E2 effects on mitochondrial biogenesis and function supporting activation of PGC1B as a therapeutic target for hepatic mitochondrial disorders.

scholarly journals Tamoxifen protects breast cancer patients from COVID-19: first evidence from real world data

2021 ◽  
Author(s):  
Sara Bravaccini ◽  
Fabio Nicolini ◽  
William Balzi ◽  
Irene Azzali ◽  
Arianna Calistri ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Protective Role ◽  
In Vitro Experiments ◽  
Breast Cancer Patients ◽  
Real World Data ◽  
17Β Estradiol ◽  
Hormonal Therapies

Abstract Background COVID-19 severity is uneven between genders. We hypothesized a role of hormonal therapies in the severity of COVID-19 in breast cancer (BC) patients via the modulation of SARS-CoV-2 susceptibility genes. Patients and Methods We mined the Emilia Romagna region (Italy) registries to compare the rates of hospitalization and mortality for COVID-19 in 2020 amongst 24628 BC patients. Next, we analyzed the modulation of ACE2, TMPRSS2 and NRP1 gene expression and the susceptibility to SARS-CoV-2 infection by tamoxifen, fulvestrant and 17β-estradiol on human ER+ MCF-7 cells in vitro.Results The hospitalization rate observed for 4784 tamoxifen treated BC patients was the lowest (OR, 0.41; 95% CI, 0.18-0.94; p=0.04) among hormonal therapies and no fatalities occurred. A standard mortality rate reduction has been observed also for patients treated with aromatase inhibitors (SMR: 0.73; 95% CI, 0.45-0.90). In vitro experiments showed that fulvestrant, but not tamoxifen, increases ACE2, TMPRSS2 and NRP1 gene expression and susceptibility to SARS-CoV-2 infection and that 17β-estradiol reduces significantly TMPRSS2 and NRP1 expression.Conclusions Tamoxifen treated BC patients showed a reduced rate of hospitalization and strikingly no fatalities for COVID-19. In vitro experiments confirmed a protective role of tamoxifen while an increased susceptibility to SARS-CoV-2 infection of ER+ cells treated with fulvestrant was observed.

Sign in / Sign up

Export Citation Format

Share Document