PUBLICATION
Bioelectric signaling and the control of cardiac cell identity in response to mechanical forces
- Authors
- Fukui, H., Chow, R.W., Xie, J., Foo, Y.Y., Yap, C.H., Minc, N., Mochizuki, N., Vermot, J.
- ID
- ZDB-PUB-211030-1
- Date
- 2021
- Source
- Science (New York, N.Y.) 374: 351-354 (Journal)
- Registered Authors
- Fukui, Hajime, Mochizuki, Naoki, Vermot, Julien
- Keywords
- none
- MeSH Terms
-
- Adenosine Triphosphate/metabolism
- Animals
- Calcium/metabolism
- Calcium Signaling
- Electrophysiological Phenomena
- Endothelial Cells/physiology
- Heart Valves/cytology
- Heart Valves/growth & development*
- Heart Valves/metabolism
- NFATC Transcription Factors/metabolism
- Receptors, Purinergic P2/metabolism
- Shear Strength*
- Stress, Mechanical*
- Zebrafish
- PubMed
- 34648325 Full text @ Science
Citation
Fukui, H., Chow, R.W., Xie, J., Foo, Y.Y., Yap, C.H., Minc, N., Mochizuki, N., Vermot, J. (2021) Bioelectric signaling and the control of cardiac cell identity in response to mechanical forces. Science (New York, N.Y.). 374:351-354.
Abstract
Developing cardiovascular systems use mechanical forces to take shape, but how ubiquitous blood flow forces instruct local cardiac cell identity is still unclear. By manipulating mechanical forces in vivo, we show here that shear stress is necessary and sufficient to promote valvulogenesis. We found that valve formation is associated with the activation of an extracellular adenosine triphosphate (ATP)–dependent purinergic receptor pathway, specifically triggering calcium ion (Ca2+) pulses and nuclear factor of activated T cells 1 (Nfatc1) activation. Thus, mechanical forces are converted into discrete bioelectric signals by an ATP-Ca2+-Nfatc1–mechanosensitive pathway to generate positional information and control valve formation.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping