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Published on: August 13, 2019
VWF and ADAMTS13 behavior in estradiol-treated HUVEC
Yanina Powazniak1, Ana Catalina Kempfer, Julio César Calderazzo Pereyra
1FONCyT/CONICET, Instituto de Investigaciones Hematológicas, Academia Nacional de Medicina, Buenos Aires, Argentina. yaninapowazniak@gmail.com
European Journal of Haematology
|October 21, 2010
Summary
17β-estradiol (E2) increases intracellular ADAMTS13 production and regulates von Willebrand factor (VWF) and ADAMTS13 gene expression in human endothelial cells. This suggests a mechanism for E2
Area of Science:
- Endocrinology and Molecular Biology
- Vascular Biology and Thrombosis
Background:
- 17β-estradiol (E2) is a key hormone influencing cardiovascular health.
- Von Willebrand factor (VWF) and ADAMTS13 are critical proteins in hemostasis and thrombosis.
- Endothelial cells play a central role in regulating VWF and ADAMTS13.
Purpose of the Study:
- To investigate the role of 17β-estradiol (E2) in the regulation of VWF and ADAMTS13 synthesis, storage, and secretion.
- To explore the impact of E2 on VWF and ADAMTS13 gene expression and protein production in human umbilical vein endothelial cells (HUVEC).
Main Methods:
- HUVEC were treated with E2 (1 nm) or vehicle.
- VWF and ADAMTS13 levels were measured in cell lysates and supernatants using VWF:Ag, multimeric analysis, and SDS-PAGE.
- Gene expression of VWF and ADAMTS13 was quantified by real-time PCR.
- ADAMTS13 function was assessed via knockdown using shRNA.
Main Results:
- E2 did not alter VWF release or intracellular levels.
- E2 significantly increased intracellular ADAMTS13 production and mRNA expression for both VWF and ADAMTS13.
- Knockdown of ADAMTS13 upregulated VWF release and intracellular levels in E2-treated HUVEC.
Conclusions:
- E2 regulates VWF and ADAMTS13 gene expression and production in human endothelial cells.
- Intracellular regulation of VWF by ADAMTS13 may mediate the cardiovascular protective effects of E2.
- These findings elucidate a novel mechanism for E2's role in vascular health.

