ArticleVascular pharmacology
Effects of 17 β-estradiol on lipopolysacharride-induced intracellular adhesion molecule-1 mRNA expression and Ca²+ homeostasis alteration in human endothelial cells.
Article in Vascular pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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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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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Associations Between Follicular Fluid Biomarkers and IVF/ICSI Outcomes in Normo-Ovulatory Women-A Systematic Review.Biomolecules · 2025Pooled it
- Regional Diversities in Fibrogenesis Weighed as a Key Determinant for Atrial Arrhythmogenesis.Biomedicines · 2021Review
- Neutrophil-to-Lymphocyte Ratio as a Cardiovascular Risk Marker May Be Less Efficient in Women Than in Men.Biomolecules · 2021Review
- Alcohol Drinking, Apolipoprotein Polymorphisms and the Risk of Cardiovascular Diseases.Current neurovascular research · 2021Review
- The Impact of Estrogen Receptor in Arterial and Lymphatic Vascular Diseases.International journal of molecular sciences · 2020Review
- Sex as a Biological Variable in Atherosclerosis.Circulation research · 2020Review
- Sex differences in vascular physiology and pathophysiology: estrogen and androgen signaling in health and disease.American journal of physiology. Heart and circulatory physiology · 2017Review
- Lipopolysaccharide induces endoplasmic store Ca2+-dependent inflammatory responses in lung microvessels.PloS one · 2013Article
- Sex differences in creatine kinase after acute heavy resistance exercise on circulating granulocyte estradiol receptors.European journal of applied physiology · 2012Article
Corrections and comments
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Authors and funding
6 authors.
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Abstract
Recent evidence showed that 17 β-estradiol (E₂) decreased cytokine-induced expression of cell adhesion molecules (CAM). Changes in intracellular Ca²+ concentration ([Ca²+](i)) has been shown to be associated with CAM expression in endothelial cells. Here, the effects of E₂ (1 μM, 24 h) on the expression of intracellular adhesion molecule-1 (ICAM-1) and [Ca²+](i) were investigated in a lipopolysaccharide (LPS) (100 ng/mL, 18 h)-stimulated human endothelial cell line, EA.hy926, using real-time PCR and spectrofluorometry, respectively. PCR analysis revealed a significant increase in ICAM-1 expression in calcium ionophore A23187 (1 nM)- or LPS-stimulated cells. Pretreatment of cells with E(2) significantly inhibited LPS-induced ICAM-1 mRNA expression. [Ca²+](i) was monitored in Fura-2AM-loaded cells in the presence and absence of extracellular Ca²+ with thapsigargin (TG, 1 μM), a sarco/endoplasmic reticulum ATPase inhibitor or ATP (100 μM). The extent of TG- or ATP-induced [Ca²+](i) increase was significantly higher in LPS-stimulated cells than in control cells. Pre-treatment of LPS-stimulated cells with E₂ limited the Ca²+ response to the same level as in control cells. Furthermore, ICI 182,780, an estrogen receptor antagonist, attenuated the inhibitory actions of E₂ on ICAM-1 mRNA expression and Ca²+ responses, suggesting that estrogen receptors mediate, at least in part, the effects of estrogen. These data suggest a potential underlying mechanism for the protective effect of E₂ against atherosclerosis.
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Registered trials
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