ArticlePloS one2023
High risk oral contraceptive hormones do not directly enhance endothelial cell procoagulant activity in vitro.
Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- An Integrated Approach Combining Chemical Profiling, Network Pharmacology, and Experimental Validation Is Used to Clarify the Pharmacological Basis of the Yiqi-Tongluo-Huoxue-Mingmu Formula in Diabetic Retinopathy.Journal of diabetes research · 2026Article
- Combined Oral Contraceptives and the Risk of Thrombosis.International journal of molecular sciences · 2025Review
- A cell-based model to study mechanisms of endothelial-dependent thrombin generation in response to inflammation and its modulation by hydroxychloroquine.Research and practice in thrombosis and haemostasis · 2025Article
- Hormone-induced thrombosis is mediated through non-canonical fibrin(ogen) aggregation and a novel estrogen target in zebrafish.bioRxiv : the preprint server for biology · 2024Article
- Hormonal and laboratory predictors of patent foramen ovale in cryptogenic ischemic events: a SHAP-enhanced logistic regression approach.Frontiers in neurologyArticle
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundOral contraceptive (OC) use increases venous thromboembolism risk 2-5-fold. Procoagulant changes can be detected in plasma from OC users even without thrombosis, but cellular mechanisms that provoke thrombosis have not been identified. Endothelial cell (EC) dysfunction is thought to initiate venous thromboembolism. It is unknown whether OC hormones provoke aberrant procoagulant activity in ECs.
objectiveCharacterize the effect of high-risk OC hormones (ethinyl estradiol [EE] and drospirenone) on EC procoagulant activity and the potential interplay with nuclear estrogen receptors ERα and ERβ and inflammatory processes.
methodsHuman umbilical vein and dermal microvascular ECs (HUVEC and HDMVEC, respectively) were treated with EE and/or drospirenone. Genes encoding the estrogen receptors ERα and ERβ (ESR1 and ESR2, respectively) were overexpressed in HUVEC and HDMVEC via lentiviral vectors. EC gene expression was assessed by RT-qPCR. The ability of ECs to support thrombin generation and fibrin formation was measured by calibrated automated thrombography and spectrophotometry, respectively.
resultsNeither EE nor drospirenone, alone or together, changed expression of genes encoding anti- or procoagulant proteins (TFPI, THBD, F3), integrins (ITGAV, ITGB3), or fibrinolytic mediators (SERPINE1, PLAT). EE and/or drospirenone did not increase EC-supported thrombin generation or fibrin formation, either. Our analyses indicated a subset of individuals express ESR1 and ESR2 transcripts in human aortic ECs. However, overexpression of ESR1 and/or ESR2 in HUVEC and HDMVEC did not facilitate the ability of OC-treated ECs to support procoagulant activity, even in the presence of a pro-inflammatory stimulus.
conclusionsThe OC hormones EE and drospirenone do not directly enhance thrombin generation potential of primary ECs in vitro.
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