High risk oral contraceptive hormones do not directly enhance endothelial cell procoagulant activity in vitro.

ABSTRACT:

Background

Oral 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.

Objective

Characterize 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.

Methods

Human umbilical vein and dermal microvascular ECs (HUVEC and HDMVEC, respectively) were treated with EE and/or drospirenone. Genes e

SUBMITTER: Bouck EG 

PROVIDER: S-EPMC10115293 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature