PUBLICATION
An injury-responsive mmp14b enhancer is required for heart regeneration
- Authors
- Zlatanova, I., Sun, F., Wu, R.S., Chen, X., Lau, B.H., Colombier, P., Sinha, T., Celona, B., Xu, S.M., Materna, S.C., Huang, G.N., Black, B.L.
- ID
- ZDB-PUB-231130-4
- Date
- 2023
- Source
- Science advances 9: eadh5313eadh5313 (Journal)
- Registered Authors
- Black, Brian, Celona, Barbara, Chen, Xiaoxin Luke, Sun, Fei
- Keywords
- none
- Datasets
- GEO:GSE211424
- MeSH Terms
-
- Animals
- Cell Proliferation
- Endothelial Cells*
- Mammals
- Mice
- Myocardium/metabolism
- Myocytes, Cardiac/metabolism
- Regeneration
- Zebrafish*
- PubMed
- 38019918 Full text @ Sci Adv
Citation
Zlatanova, I., Sun, F., Wu, R.S., Chen, X., Lau, B.H., Colombier, P., Sinha, T., Celona, B., Xu, S.M., Materna, S.C., Huang, G.N., Black, B.L. (2023) An injury-responsive mmp14b enhancer is required for heart regeneration. Science advances. 9:eadh5313eadh5313.
Abstract
Mammals have limited capacity for heart regeneration, whereas zebrafish have extraordinary regeneration abilities. During zebrafish heart regeneration, endothelial cells promote cardiomyocyte cell cycle reentry and myocardial repair, but the mechanisms responsible for promoting an injury microenvironment conducive to regeneration remain incompletely defined. Here, we identify the matrix metalloproteinase Mmp14b as an essential regulator of heart regeneration. We identify a TEAD-dependent mmp14b endothelial enhancer induced by heart injury in zebrafish and mice, and we show that the enhancer is required for regeneration, supporting a role for Hippo signaling upstream of mmp14b. Last, we show that MMP-14 function in mice is important for the accumulation of Agrin, an essential regulator of neonatal mouse heart regeneration. These findings reveal mechanisms for extracellular matrix remodeling that promote heart regeneration.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping