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MicroRNAs differentially expressed in postnatal aortic development downregulate elastin via 3' UTR and

Claus Eric Ott¹, Johannes Grünhagen, Marten Jäger

¹Institute for Medical Genetics, Charité-Universitätsmedizin Berlin, Berlin, Germany.

|February 10, 2011

Summary

MicroRNAs (miRNAs) like miR-29 and miR-15 regulate gene expression. These miRNAs are upregulated during aorta development, downregulating elastin and extracellular matrix (ECM) gene production.

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Area of Science:

Molecular Biology
Developmental Biology
Genetics

Background:

Elastin production ceases during the maturation of elastin-rich organs like the aorta.
MicroRNAs (miRNAs) are small regulatory RNAs that control gene expression by targeting messenger RNAs (mRNAs).
miRNA regulatory elements (MREs) are typically found in the 3' untranslated region (UTR) of mRNAs.

Purpose of the Study:

To investigate the role of specific miRNAs in regulating elastin and extracellular matrix (ECM) gene expression during aortic development.
To identify and characterize miRNA regulatory elements (MREs) in elastin and other ECM genes.
To elucidate the mechanism by which miRNAs contribute to the downregulation of elastin in the adult aorta.

Main Methods:

Analysis of miRNA expression during murine aortic development.
Bioinformatic identification of MREs in elastin and ECM genes.
Luciferase reporter assays to validate miRNA-target interactions.

Main Results:

miR-29 and miR-15 family miRNAs were significantly upregulated during murine aortic development.
A high number of MREs for miR-29 were found in the coding sequences (CDS) and 3' UTR of elastin, and in other ECM genes including collagens.
Luciferase assays confirmed synergistic effects of miR-29 and miR-15 family miRNAs on elastin constructs, indicating functional regulation.

Conclusions:

Multiple MREs for miR-29 and miR-15 family miRNAs are characteristic features of certain ECM genes.
These miRNAs are implicated in the developmental downregulation of elastin in the adult aorta.
The findings highlight a conserved mechanism of gene regulation in mammalian aortic development.