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Analysis of Cardiomyocyte Development using Immunofluorescence in Embryonic Mouse Heart
Published on: March 26, 2015
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SIRT1 regulates cardiomyocyte alignment during maturation
Yi Fang1, Wei Fan1, Xiaojiang Xu2
1Signal Transduction Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA.
Journal of Cell Science
|March 9, 2022
Summary
Sirtuin 1 (SIRT1) is crucial for cardiomyocyte alignment and heart development. SIRT1 deficiency disrupts cardiomyocyte organization and function, impacting cardiac maturation.
Area of Science:
- Cardiovascular Biology
- Developmental Biology
- Molecular Cardiology
Background:
- Cardiomyocyte alignment is essential for proper heart function, enabling organized contraction.
- The molecular mechanisms controlling cardiomyocyte alignment during development are not fully understood.
Purpose of the Study:
- To investigate the role of Sirtuin 1 (SIRT1) in regulating cardiomyocyte alignment and cardiac remodeling during development.
Main Methods:
- Utilized an in vitro differentiation system using human embryonic stem cells.
- Generated SIRT1-deficient mouse models at late developmental stages.
- Analyzed cardiomyocyte/myofibril alignment, beating patterns, and gene expression related to chemotaxis pathways (CXCL12/CXCR4, CCL2/CCR2/CCR4).
Main Results:
- SIRT1 deficiency in vitro impaired cardiomyocyte/myofibril alignment and disrupted beating patterns.
- SIRT1 deletion in mouse embryos led to irregular cardiomyocyte distribution, myofibril misalignment, and reduced heart size.
- SIRT1 deficiency blunted the expression of key chemotaxis genes, and CCL2 signaling inhibition reduced cardiomyocyte alignment.
Conclusions:
- SIRT1 plays a critical role in controlling cardiomyocyte alignment at the inter-cellular level during cardiac maturation.
- SIRT1 influences cardiac development by regulating gene expression in chemotaxis pathways, impacting cardiomyocyte organization and heart size.
