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Related Experiment Video

Updated: Jun 17, 2026

In Vitro Model of Fetal Human Vessel On-chip to Study Developmental Mechanobiology

In Vitro Model of Fetal Human Vessel On-chip to Study Developmental Mechanobiology

Published on: July 28, 2023

Hemodynamic forces regulate embryonic stem cell commitment to vascular progenitors.

Tzung K Hsiai¹, Joseph C Wu

¹Department of Biomedical Engineering and Division of Cardiovascular Medicine, University of Southern California, Los Angeles, CA 90089-1111, USA.

Current Cardiology Reviews

|January 13, 2010

Summary

This summary is machine-generated.

Fluid shear stress promotes embryonic stem cell differentiation into vascular progenitor cells, crucial for blood vessel repair and engineering. Understanding these hemodynamic forces aids in developing therapeutic strategies for vascular damage.

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Isolation of Murine Embryonic Hemogenic Endothelial Cells

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Published on: June 17, 2016

Area of Science:

Stem Cell Biology
Cardiovascular Research
Biomedical Engineering

Background:

Embryonic stem (ES) cells possess pluripotency, differentiating into all cell types.
Embryonic development involves exposure to hemodynamic forces, like fluid flow, essential for proper cardiac formation.
Absence of fluid flow leads to abnormal cardiac chamber and valve development.

Purpose of the Study:

To investigate the role of hemodynamic forces, specifically fluid shear stress, in ES cell differentiation.
To explore the potential of ES cell-derived vascular progenitor cells (VPCs) for therapeutic applications in vascular repair and engineering.
To understand the kinetics of ES cell differentiation towards the endothelial lineage under fluid shear stress.

Main Methods:

Exposure of pluripotent embryonic stem cells to controlled fluid shear stress.
Analysis of cell cycle progression (S and G(2)-M phases) and chromatin structure.
Quantification of CD31(+) vascular progenitor cell commitment and characterization of their endothelial markers (eNOS, vWF) and functions (LDL uptake, network formation).

Main Results:

Fluid shear stress increased the percentage of cells in S and G(2)-M phases, promoting gene transcription.
Shear stress accelerated ES cell commitment to CD31(+) VPCs.
ES-derived CD31(+) cells exhibited endothelial markers (eNOS, vWF) and functional capabilities like LDL uptake and tubular network formation.

Conclusions:

Hemodynamic forces, particularly fluid shear stress, are critical regulators of ES cell differentiation into endothelial lineage.
ES-derived CD31(+) VPCs hold significant therapeutic potential for vascular damage repair and engineered vascular grafts.
A multidisciplinary approach is essential to overcome challenges in producing pure, stable, and non-tumorigenic endothelial progenitors for clinical applications.