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Transcription profiling of mice hearts comparing microRNA-22 KO to wildtype

ABSTRACT: To explore the role of miR-22 in the heart, we generated miR-22 null and transgenic mice. Absence of miR-22 results in partial embryonic lethality arising from cardiac malformations. miR-22-null mice that survived until adulthood showed normal cardiac structure and function at baseline but were sensitized to cardiac dysfunction and dilation following pressure overload stimulation. Absence of miR-22 prevented the induction of beta-myosin heavy chain (Myh7) and miR-208b expression following pathologic stress. miR-22 null animals were also compromised in cardiac expression of Myh7b and miR-499. We found that miR-22 directly regulates two transcriptional antagonists, purine rich element binding protein B (PURB), a repressor, and serum response factor (SRF), an activator, in the heart. Through these gain- and loss-of-function experiments in mice, we suggest that a primary function of miR-22 is to fine tune the relative expression and activity of these two transcriptional antagonists to influence contractile gene expression, function, growth and adaptation of the heart to stress.

ORGANISM(S): Mus musculus

SUBMITTER: Cei Abreu-Goodger

PROVIDER: E-MTAB-500 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcription profiling of mice hearts comparing microRNA-22 overexpression to wildtype

Project description:To explore the role of miR-22 in the heart, we generated miR-22 null and transgenic mice. Cardiac transgenic overexpression of miR-22 in vivo led to cardiac hypertrophy that evolved into progressive dilated cardiomyopathy (DCM) in unstressed hearts. We found that miR-22 directly regulates two transcriptional antagonists, purine rich element binding protein B (PURB), a repressor, and serum response factor (SRF), an activator, in the heart. Through these gain- and loss-of-function experiments in mice, we suggest that a primary function of miR-22 is to fine tune the relative expression and activity of these two transcriptional antagonists to influence contractile gene expression, function, growth and adaptation of the heart to stress.

2012-12-01 | E-MTAB-501 | biostudies-arrayexpress

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2014-03-06 | E-MTAB-2038 | biostudies-arrayexpress

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