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Related Experiment Video

Updated: May 30, 2025

In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time

In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time

Published on: May 24, 2020

ENDOTHELIAL-SPECIFIC KNOCKOUT OF THE SCRAMBLASE TMEM16F IMPAIRS IN VIVO CLOT FORMATION.

Grace Bonson¹, Aaron R Lambert¹, Adrian M Sackheim¹

¹Department of Emergency Medicine, University of Vermont, Burlington, Vermont.

Shock (Augusta, Ga.)

|January 28, 2025

Summary

This summary is machine-generated.

Endothelial TMEM16F is crucial for normal hemostasis. Mice lacking TMEM16F in endothelial cells showed prolonged bleeding and reduced clot formation, indicating its role in preventing bleeding disorders.

Keywords:

Mouse blood vessels coagulopathy endothelium hemostasis phosphatidylserine scramblase thrombosis

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Area of Science:

Vascular Biology
Hemostasis and Thrombosis
Cellular Physiology

Background:

Loss of phospholipid scramblase (PLS) TMEM16F function causes Scott syndrome, a bleeding disorder linked to platelet dysfunction.
The specific role of TMEM16F in endothelial cells remains largely unexplored.

Purpose of the Study:

To investigate the contribution of endothelial TMEM16F to hemostasis.
To test if TMEM16F in endothelial cells is essential for regulating bleeding time and venous clotting.

Main Methods:

Pharmacological inhibition of TMEM16F in cultured endothelial cells exposed to histones, assessing calcium signaling and phosphatidylserine translocation.
Generation of endothelial-specific TMEM16F knockout (ECKO) mice using a tamoxifen-inducible cre-lox system.
Evaluation of hemostasis via tail bleeding time and inferior vena cava (IVC) stenosis-induced thrombus formation.
Assessment of plasma coagulation and endothelial-dependent vasodilation.

Main Results:

Inhibition of TMEM16F prevented pathological calcium signals and phosphatidylserine translocation in endothelial cells.
TMEM16F ECKO mice exhibited significantly prolonged bleeding times and reduced IVC thrombus size compared to controls.
TMEM16F ablation did not affect prothrombin time or endothelial vasodilation.

Conclusions:

Endothelial TMEM16F plays a critical role in maintaining normal hemostasis.
Ablation of TMEM16F specifically in endothelial cells results in a coagulopathic phenotype.
These findings suggest TMEM16F's involvement in trauma-induced coagulopathy due to its role in endothelial calcium signaling.