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miR-486 is modulated by stretch and increases ventricular growth

Artikel i vetenskaplig tidskrift
Författare Stephan Lange
I. Banerjee
K. Carrion
R. Serrano
L. Habich
R. Kameny
L. Lengenfelder
N. Dalton
R. Meili
Emma Börgeson
K. Peterson
M. Ricci
J. Lincoln
M. Ghassemian
J. Fineman
J. C. del Alamo
V. Nigam
Publicerad i Jci Insight
Volym 4
Nummer/häfte 19
ISSN 2379-3708
Publiceringsår 2019
Publicerad vid Wallenberglaboratoriet
Språk en
Länkar dx.doi.org/10.1172/jci.insight.1255...
Ämnesord congenital heart-disease, serum response factor, mechanical stretch, transcription factor, cardiac-hypertrophy, gene-expression, aortic-valve, proliferation, inhibition, micrornas, Research & Experimental Medicine
Ämneskategorier Kardiologi

Sammanfattning

Perturbations in biomechanical stimuli during cardiac development contribute to congenital cardiac defects such as hypoplastic left heart syndrome (HLHS). This study sought to identify stretch-responsive pathways involved in cardiac development. miRNA-Seq identified miR-486 as being increased in cardiomyocytes exposed to cyclic stretch in vitro. The right ventricles (RVs) of patients with HLHS experienced increased stretch and had a trend toward higher miR-486 levels. Sheep RVs dilated from excessive pulmonary blood flow had 60% more miR-486 compared with control RVs. The left ventricles of newborn mice treated with miR-486 mimic were 16.9%-24.6% larger and displayed a 2.48-fold increase in cardiomyocyte proliferation. miR-486 treatment decreased Fox01 and Smad signaling while increasing the protein levels of Stat1. Stat1 associated with Gata-4 and serum response factor (Srf), 2 key cardiac transcription factors with protein levels that increase in response to miR-486. This is the first report to our knowledge of a stretch-responsive miRNA that increases the growth of the ventricle in vivo.

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