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Regulation of zebrafish heart regeneration by miR-133

Open access
Yin, Viravuth P., Lepilina, Alexandra, Smith, Ashley, Poss, Kenneth D.·2012·Developmental Biology

Abstract

Zebrafish regenerate cardiac muscle after severe injuries through the activation and proliferation of spared cardiomyocytes. Little is known about factors that control these events. Here we investigated the extent to which miRNAs regulate zebrafish heart regeneration. Microarray analysis identified many miRNAs with increased or reduced levels during regeneration. miR-133, a miRNA with known roles in cardiac development and disease, showed diminished expression during regeneration. Induced transgenic elevation of miR-133 levels after injury inhibited myocardial regeneration, while transgenic miR-133 depletion enhanced cardiomyocyte proliferation. Expression analyses indicated that cell cycle factors mps1, cdc37, and PA2G4, and cell junction components cx43 and cldn5, are miR-133 targets during regeneration. With pharmacological inhibition and EGFP sensor interaction studies, we demonstrated that cx43 is a new miR-133 target and regeneration gene. Our results reveal dynamic regulation of miRNAs during heart regeneration, and indicate that miR-133 restricts injury-induced cardiomyocyte proliferation.

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Metadata

Authors
Yin, V. P., Lepilina, A., Smith, A., & Poss, K. D.
Venue
Developmental Biology
Publisher
Elsevier BV
Published
2012-05
Volume
365
Issue
2
Pages
319-327
ISSN
0012-1606 (ISSN-L)
OpenAlex
W1997529197
Cited by
195
References
4
FWCI
8.25
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Regulation of zebrafish heart regeneration by miR-133. https://app.cochat.ai/papers/10.1016/j.ydbio.2012.02.018
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Yin, V. P., Lepilina, A., Smith, A., & Poss, K. D. (2012). Regulation of zebrafish heart regeneration by miR-133. Developmental Biology. https://doi.org/10.1016/j.ydbio.2012.02.018

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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