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Related Experiment Video

Updated: Jul 2, 2025

Gene Expression Analysis of Endothelial Cells Exposed to Shear Stress Using Multiple Parallel-plate Flow Chambers

Gene Expression Analysis of Endothelial Cells Exposed to Shear Stress Using Multiple Parallel-plate Flow Chambers

Published on: October 21, 2018

Epigenetic changes in shear-stressed endothelial cells.

Thaís Silva Pinto¹, Geórgia da Silva Feltran¹, Célio Júnior da C Fernandes¹

¹Lab. of Bioassays and Cellular Dynamics, Department of Chemical and Biological Sciences, Institute of Biosciences, Paulista State University-UNESP, Botucatu, São Paulo, Brazil.

Cell Biology International

|February 29, 2024

Summary

High blood flow shear stress alters endothelial cell epigenetics, decreasing key histone marks and impacting HOXA13 gene expression. This reveals new insights into vascular biology and hypertension.

Keywords:

HOTTIP HOXA13 endothelial cell epigenetics hypertension shear stress

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Area of Science:

Vascular Biology
Epigenetics
Mechanobiology

Background:

Endothelial cell phenotype is regulated by epigenetic changes, particularly histone modifications, in response to blood flow forces.
The specific epigenetic mechanisms governing endothelial cell behavior under shear stress are not well understood.

Purpose of the Study:

To investigate the epigenetic modifications in endothelial cells under varying shear stress conditions.
To elucidate the role of histone modifications and gene expression changes in response to simulated hypertensive forces.

Main Methods:

In vitro experiments using human umbilical vein endothelial cells.
Subjecting cells to controlled tensional forces simulating normotensive and hypertensive blood flow.
Assessing epigenetic marks (H3K4ac, H3K27ac), histone deacetylase (HDAC) protein levels, and gene/lncRNA expression (HOXA13, HOTTIP).

Main Results:

High shear stress led to decreased H3K4ac and H3K27ac epigenetic marks.
Significant alterations in histone deacetylase (HDAC) protein levels were observed.
Increased shear stress negatively regulated HOXA13 gene expression and increased HOTTIP long noncoding RNA expression.

Conclusions:

This study provides the first evidence linking histone modifications and chromatin compaction to endothelial cell mechanosignaling under elevated shear stress.
Findings highlight the role of HOXA13 in vascular biology and hypertension, suggesting potential therapeutic targets.
Results open avenues for developing small molecules to modulate epigenetic mechanisms in hypertensive conditions.