Protective role of 17Β-estradiol in apoptosis of skeletal muscle

Abstract Angiotensin converting enzyme-2 (ACE2) is a multifunctional transmembrane protein recently recognised as the entry receptor of the virus causing COVID-19. In the renin–angiotensin system (RAS), ACE2 cleaves angiotensin II (Ang II) into angiotensin 1-7 (Ang 1-7), which is considered to exert cellular responses to counteract the activation of the RAS primarily through a receptor, Mas, in multiple organs including skeletal muscle. Previous studies have provided abundant evidence suggesting that Ang 1-7 modulates multiple signalling pathways leading to protection from pathological muscle remodelling and muscle insulin resistance. In contrast, there is relatively little evidence to support the protective role of ACE2 in skeletal muscle. The potential contribution of endogenous ACE2 to the regulation of Ang 1-7-mediated protection of these muscle pathologies is discussed in this review. Recent studies have suggested that ACE2 protects against ageing-associated muscle wasting (sarcopenia) through its function to modulate molecules outside of the RAS. Thus, the potential association of sarcopenia with ACE2 and the associated molecules outside of RAS is also presented herein. Further, we introduce the transcriptional regulation of muscle ACE2 by drugs or exercise, and briefly discuss the potential role of ACE2 in the development of COVID-19.

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Protective Role of Polysaccharides from Gynostemma pentaphyllum Makino Supplementation against Exhaustive Swimming Exercise-Induced Oxidative Stress in Liver and Skeletal Muscle of Mice

Advanced Materials Research ◽

10.4028/www.scientific.net/amr.962-965.1231 ◽

2014 ◽

Vol 962-965 ◽

pp. 1231-1234

Author(s):

Hui Huang ◽

Bo Qi

Keyword(s):

Oxidative Stress ◽

Skeletal Muscle ◽

Protective Role ◽

Swimming Exercise ◽

Control Group ◽

High Dose ◽

Gynostemma Pentaphyllum ◽

Exercise Induced ◽

Different Doses

The objective of this study was to investigate the protective role of polysaccharide fromGynostemma pentaphyllumMakino (PGP) supplementation against exhaustive swimming exercise-induced oxidative stress. A total of 48 mice were randomly divided into four groups: control, low-dose, medium-dose, and high-dose PGP supplementation groups. The control group received distilled water and the supplementation groups received different doses of PGP (50, 100 and 200 mg/kg body weight) by gavage once a day for 28 consecutive days. After 28 days, the mice performed an exhaustive swimming exercise, and some biochemical parameters related to oxidative stress, including superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and malondialdehyde (MDA), were measured. The results showed that PGP supplementation could increase SOD, GPx and CAT contents, as well as decrease MDA contents in the liver and skeletal muscle of mice, which suggests that PGP supplementation has a protective role against exhaustive swimming exercise-induced oxidative stress.

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

International Journal of Developmental Neuroscience ◽

10.1016/j.ijdevneu.2015.04.157 ◽

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

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Protective role of ischemic conditioning procedures against skeletal muscle ischemia-reperfusion injury via improving in vivo energy metabolism and mitochondrial function

Archives of Cardiovascular Diseases Supplements ◽

10.1016/s1878-6480(17)30466-4 ◽

2017 ◽

Vol 9 (2) ◽

pp. 188

Author(s):

A. Delgove ◽

D. Detaille ◽

J. Retortillo Garcia ◽

J. Magat ◽

V. Loyer ◽

...

Keyword(s):

Skeletal Muscle ◽

Energy Metabolism ◽

Mitochondrial Function ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Protective Role ◽

Ischemic Conditioning ◽

Muscle Ischemia

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

Journal of Endocrinology ◽

10.1530/joe-16-0350 ◽

2017 ◽

Vol 232 (2) ◽

pp. 297-308 ◽

Cited By ~ 14

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.

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

10.21203/rs.3.rs-598923/v1 ◽

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.

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