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Nonmuscle myosin 2 regulates cortical stability during sprouting angiogenesis
Xuefei Ma1, Yutaka Uchida2, Tingyi Wei1
1Laboratory of Molecular Cardiology, National Institutes of Health, Bethesda, MD 20892-1762.
Molecular Biology of the Cell
|June 26, 2020
Summary
Nonmuscle myosin 2A (NM2A) is crucial for blood vessel formation by stabilizing endothelial cells. Its absence leads to abnormal vascular development, highlighting NM2A
Area of Science:
- Vascular Biology
- Cell Biology
- Biochemistry
Background:
- Endothelial cells form blood vessels, a process vital for development and health.
- Nonmuscle myosin 2 (NM2) isoforms (NM2A, NM2B, NM2C) have distinct cellular roles.
- NM2A and NM2B are present in endothelial cells, suggesting a role in vascularization.
Purpose of the Study:
- To investigate the specific roles of NM2A and NM2B in endothelial cell-driven vascular formation.
- To elucidate the molecular mechanisms by which NM2 regulates angiogenic sprouting.
Main Methods:
- Genetic ablation of NM2 paralogs in endothelial cells of mice.
- Analysis of developing skin and coronary vasculature in knockout mouse models.
- In vitro angiogenic sprouting assay using embryoid bodies in collagen gels.
Main Results:
- Endothelial-specific ablation of NM2A, but not NM2B, impaired vascular coverage and increased branching.
- NM2B function is critical for vascularization when NM2A is limited.
- NM2A stabilizes the endothelial cell cortex, promoting persistent migration and preventing excessive sprouting.
- NM2 signaling regulates focal adhesion and cortical protrusion dynamics during angiogenesis.
Conclusions:
- NM2A plays a primary role in stabilizing the endothelial cytoskeleton, ensuring proper vascular development.
- NM2B compensates for NM2A loss, indicating functional redundancy.
- Rho kinase-activated NM2 signaling is a key regulator of angiogenic sprouting in vitro and in vivo.
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