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| Status |
Public on Jul 17, 2023 |
| Title |
Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to the transition to heart failure (rat sample) |
| Organism |
Rattus norvegicus |
| Experiment type |
Expression profiling by high throughput sequencing
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| Summary |
Non-canonical Wnt signaling activated by Wnt5a and Wnt11 is required for the development of second heart field cardiac progenitor cells in mice. However, the pathophysiological role of non-canonical Wnt signaling in the adult heart has not been fully elucidated. Here we show that cardiomyocyte-specific Wnt5a knockout mice exhibit improved systolic function and reduced expression of mechanosensitive genes including Nppb compared to control mice when subjected to pressure overload. In cultured cardiac myocytes, Wnt5a knockdown reduces the upregulation of Nppb gene expression and YAP nuclear translocation induced by cyclic cell stretch. Wnt5a knockdown-induced Nppb downregulation in response to cell stretch is rescued by inhibition of Hippo pathway, and the rescue effect of Hippo inhibition is canceled by YAP knockdown. These results collectively suggest that Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to the transition to heart failure.
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| Overall design |
mRNA profiles obtained from neonatal rat ventricular cardiomyocytes
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| Contributor(s) |
Iwasaki M, Okuzaki D, Motooka D |
| Citation(s) |
37456848 |
| Submission date |
Apr 12, 2022 |
| Last update date |
Jun 06, 2024 |
| Contact name |
Daisuke Motooka |
| E-mail(s) |
dry_team@ngs.gen-info.osaka-u.ac.jp
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| Organization name |
NGS core facility, Research Institute for Microbial Diseases, Osaka University
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| Street address |
3-1, Yamadaoka
|
| City |
Suita |
| State/province |
Osaka |
| ZIP/Postal code |
5650871 |
| Country |
Japan |
| |
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| Platforms (1) |
| GPL18694 |
Illumina HiSeq 2500 (Rattus norvegicus) |
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| Samples (12)
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| This SubSeries is part of SuperSeries: |
| GSE200667 |
Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to the transition to heart failure |
|
| Relations |
| BioProject |
PRJNA825767 |
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