ArticleMolecular and cellular biochemistry2013
Estradiol inhibits vascular endothelial cells pro-inflammatory activation induced by C-reactive protein.
Article in Molecular and cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 19 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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Who cites it
19 citing papers in PubMed, 37 citations in OpenAlex.
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- Hallmarks of Cancer Cachexia: Sexual Dimorphism in Related Pathways.International journal of molecular sciences · 2025Review
- Effect of 17β-Estradiol on Endothelial Cell Expression of Inflammation- Related MicroRNA.MicroRNA (Shariqah, United Arab Emirates) · 2025Article
- Estrogen-immuno-neuromodulation disorders in menopausal depression.Journal of neuroinflammation · 2024Review
- Estrogen: the forgotten player in metaflammation.Frontiers in pharmacology · 2024Review
- Unilateral posterior reversible encephalopathy syndrome characterized with a long and gradually exacerbating course over 3 years and that presented propofol infusion syndrome - A case report.Surgical neurology international · 2021Article
- Selected sex related differences in pathophysiology of cardiovascular system.Physiological research · 2020Review
- Endothelial Cell Metabolism.Physiological reviews · 2018Review
- The effects of oestrogens and their receptors on cardiometabolic health.Nature reviews. Endocrinology · 2017Review
- Ovarian function's role during cancer cachexia progression in the female mouse.American journal of physiology. Endocrinology and metabolism · 2017Article
- Familial Mediterranean Fever With Complete Symptomatic Remission During Pregnancy.Intestinal research · 2015Article
- Sex differences in the relationship of IL-6 signaling to cancer cachexia progression.Biochimica et biophysica acta · 2015Article
- Antioxidant response of osteoblasts to doxycycline in an inflammatory model induced by C-reactive protein and interleukin-6.Infectious disorders drug targets · 2014Article
- The expression of inflammatory cytokines on the aorta endothelia are up-regulated in pinealectomized rats.Inflammation · 2013Article
- Flaxseed prevents leukocyte and platelet adhesion to endothelial cells in experimental atherosclerosis by reducing sVCAM-1 and vWF.TheScientificWorldJournal · 2013Article
Corrections and comments
- Expression of concern
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In addition of being an important inflammatory biomarker and a risk factor for cardiovascular disease, much evidence indicates that the C-reactive protein (CRP) contributes to the atherosclerosis development process. This plasmatic protein synthesized by hepatocytes in response to inflammation and tissue injury induces pro-inflammatory molecules' expression by endothelial cells (ECs). Previous studies showed that the 17β-estradiol (E2) has beneficial effects on vascular cells by reducing in vitro pro-inflammatory molecules expressions in EC. Therefore, we hypothesize that E2 blocks or reduces CRP-mediated inflammatory responses by modulating endogenous production of CRP in EC and/or activation mechanisms. Using human aortic ECs (HAECs), we first evaluated CRP production by vascular EC and second demonstrated its self-induction. Indeed, recombinant human CRP stimulation induces a fivefold increase of CRP expression. A 1-h pre-treatment of E2 at a physiologic dose (10(-9 )M) leads to an important decrease of CRP production suggesting a partial blockage of its amplification loop mechanism. Furthermore, in HAEC, E2 reduces the secretion of the most potent agonist of CRP induction, the IL-6, by 21 %. E2 pre-treatment also decreased the expression of pro-inflammatory molecules IL-8, VCAM-1, and ICAM-1 induced by CRP and involved in leukocytes recruitment. In addition, we demonstrated that E2 could restore vascular endothelial growth factor-mediated EC migration response impaired by CRP suggesting another pro-angiogenic property of this hormone. These findings suggest that E2 can interfere with CRP pro-inflammatory effects via activation signals using its rapid, non-genomic pathway that may provide a new mechanism to improve vascular repair.
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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.