ArticleMolecular and cellular endocrinology2014
17β-Estradiol alters oxidative stress response protein expression and oxidative damage in the uterus.
Article in Molecular and cellular endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 24 citations in OpenAlex.
- The embryo-derived protein PDI is highly conserved among placental mammals and alters the endometrial transcriptome and secretome in vitro across species with differing implantation strategies†.Biology of reproduction · 2026Article
- The synergistic antibacterial activity and mechanism of colistin-oxethazaine combination against gram-negative pathogens.Frontiers in pharmacology · 2024Article
- Effect of monosodium glutamate on serum sex hormones and uterine histology in female rats along with its molecular docking andHeliyon · 2022Article
- Estradiol Regulates Txnip and Prevents Intermittent Hypoxia-Induced Vascular Injury.Scientific reports · 2017Article
- 17β-Estradiol alters oxidative damage and oxidative stress response protein expression in the mouse mammary gland.Molecular and cellular endocrinology · 2016Article
- NaCl pretreatment attenuates H.pylori-induced DNA damage and exacerbates proliferation of gastric epithelial cells (GES-1).Infectious agents and cancer · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The steroid hormone 17β-estradiol (E2) has profound effects on the uterus. However, with the E2-induced increase in uterine cell proliferation and metabolism comes increased production of reactive oxygen species (ROS). We examined the expression of an interactive network of oxidative stress response proteins including thioredoxin (Trx), Cu/Zn superoxide dismutase (SOD1), apurinic endonuclease (Ape1), and protein disulfide isomerase (PDI). We demonstrated that treatment of ovariectomized C57BL/6J female mice with E2 increased the mRNA and protein levels of Trx, but decreased SOD1 and Ape1 mRNA and protein expression. In contrast, E2 treatment increased PDI protein levels but had no effect on PDI transcript levels. Interestingly, E2 treatment also increased two markers of cellular damage, lipid peroxidation and protein carbonylation. Our studies suggest that the decreased expression of SOD1 and Ape1 caused by E2 treatment may in the long term result in disruption of ROS regulation and play a role in endometrial carcinogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.