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Estradiol-Responsive miR-365a-3p Interacts with Tissue Factor 3'UTR to Modulate Tissue Factor-Initiated Thrombin

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High estradiol levels increase blood clot risk by regulating microRNAs. Specifically, miR-365a-3p directly targets tissue factor, a key coagulation factor, influencing hypercoagulability.

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Hematology

Background:

  • Elevated estradiol (E2) is associated with increased venous thromboembolism risk, but molecular mechanisms are unclear.
  • Previous work identified an E2-responsive microRNA (miR), miR-494-3p, downregulating protein S.
  • Hypothesized that other coagulation factors, like tissue factor, are similarly regulated by miRs.

Purpose of the Study:

  • Evaluate coagulation in cohorts with high physiological estradiol (E2).
  • Characterize novel E2-responsive miRs.
  • Investigate miR regulation of tissue factor in E2-related hypercoagulability.

Main Methods:

  • Assessed plasma coagulation using Ceveron Alpha thrombin generation assay (TGA).
  • Quantified miR expression in HuH-7 cells treated with 10 nM E2 using NanoString nCounter and validated findings.
  • Confirmed miR-tissue factor interaction via dual-luciferase reporter assays, immunoblotting, flow cytometry, biochemistry, and TGA.

Main Results:

  • Pregnant women and women on contraceptive pills showed hypercoagulability compared to controls.
  • miR-365a-3p expression was downregulated by high physiological E2 levels.
  • E2 treatment upregulated tissue factor protein; miR-365a-3p directly interacted with F3-3'UTR, decreasing tissue factor mRNA, protein, activity, and thrombin generation.

Conclusions:

  • miR-365a-3p is identified as a novel regulator of tissue factor.
  • High estradiol concentrations induce a hypercoagulable state through a miR network targeting coagulation factors.