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En Face Endocardial Cushion Preparation for Planar Morphogenesis Analysis in Mouse Embryos
Published on: July 27, 2022
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Endocardial HDAC3 is required for myocardial trabeculation.
Biorxiv : the Preprint Server for Biology
|October 27, 2023
Summary
Endocardial histone deacetylase 3 (HDAC3) is crucial for heart development by promoting growth signaling. Its absence disrupts transforming growth factor β3 (TGFβ3) via microRNA-129-5p, leading to congenital heart defects.
Area of Science:
- Cardiovascular Development
- Molecular Biology
- Epigenetics
Background:
- Trabeculation is vital for heart formation, and its failure causes embryonic lethality.
- Endocardial cell support, including extracellular matrix (ECM) and growth factor secretion, is critical for trabeculation.
- Mechanisms regulating endocardial ECM and growth factor secretion remain unclear.
Approach:
- Utilized mouse models and molecular tools to investigate histone deacetylase 3 (HDAC3) in endocardial cells.
- Employed single-cell RNA sequencing and transcriptomic analysis to identify molecular changes.
- Investigated the role of microRNA-129-5p in regulating transforming growth factor β3 (TGFβ3) expression.
Key Points:
- Genetic deletion of HDAC3 in mouse endocardium caused embryonic lethality with hypotrabeculation.
- HDAC3 deficiency led to downregulated ECM components and disrupted growth signaling in cardiomyocytes.
- HDAC3 represses miR-129-5p, which in turn suppresses TGFβ3 expression, essential for myocardial growth.
Conclusions:
- Endocardial HDAC3 promotes trabecular myocardium growth by stimulating TGFβ signaling via repression of miR-129-5p.
- This pathway offers insights into congenital heart disease etiology.
- Identified potential strategies for promoting myocardial regeneration.
