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Regulatory Network Analysis in Estradiol-Treated Human Endothelial Cells.
Daniel Pérez-Cremades1, Ana B Paes1, Xavier Vidal-Gómez1
1Department of Physiology, Faculty of Medicine and Dentistry, INCLIVA Biomedical Research Institute, University of Valencia, 46010 Valencia, Spain.
International Journal of Molecular Sciences
|August 7, 2021
Summary
This study reveals how estradiol (E2) regulates endothelial cells by identifying key microRNA (miRNA) and transcription factor networks. These findings offer insights into vascular biology and estradiol
Area of Science:
- Molecular Biology
- Genomics
- Endothelial Cell Biology
Background:
- Estrogen (E2) exerts beneficial effects on vascular biology via endothelial cell actions.
- MicroRNAs (miRNAs) and transcription factors are critical regulators of gene expression and cellular signaling networks.
Purpose of the Study:
- To identify a comprehensive regulatory network (miRNA-transcription factor-downstream genes) controlling transcriptomic changes in endothelial cells exposed to estradiol.
- To elucidate the molecular mechanisms underlying estradiol's effects on endothelial function.
Main Methods:
- Integrated microarray data from 17β-estradiol (E2)-treated human umbilical vein endothelial cells (HUVEC).
- Utilized Ingenuity Pathway Analysis for miRNA-mRNA interactions and canonical pathways.
- Employed JASPAR and TRANSFAC tools within Enrichr for predicting transcription factor-regulated genes.
Main Results:
- Identified 588 miRNA-target interactions (102 miRNAs, 588 targets), with specific numbers of up/downregulated interactions.
- Highlighted key canonical pathways regulated by E2, including hypoxia signaling and Rho-mediated actin motility.
- Revealed eight regulatory networks, notably those involving JUN and REPIN1, linked to cell adhesion pathways.
Conclusions:
- This study successfully identified regulatory networks governing estradiol's impact on endothelial cells.
- Provides novel insights into the molecular mechanisms of estradiol in regulating endothelial function through miRNA-transcription factor networks.
