JunB regulates angiogenesis and neurovascular parallel alignment in mouse embryonic skin
Yasuo Yoshitomi1, Takayuki Ikeda1, Hidehito Saito1
1Department of Biochemistry, Kanazawa Medical University School of Medicine, 1-1 Daigaku, Uchinada, Kahoku-gun, Ishikawa 920-0293, Japan.
Journal of Cell Science
|January 19, 2017
Summary
JunB is a key gene in embryonic vascular development. It promotes blood vessel and nerve fiber alignment, crucial for forming new blood vessels.
Area of Science:
- Developmental Biology
- Vascular Biology
- Neuroscience
Background:
- Blood vessels and nerve fibers often grow in parallel, suggesting interactions influence vascular network development.
- The specific genes and molecular mechanisms driving these neurovascular interactions are not well understood.
Purpose of the Study:
- To identify genes activated in endothelial cells (ECs) upon interaction with neurons during vascular development.
- To elucidate the role of JunB in neurovascular interactions and embryonic vascular network formation.
Main Methods:
- Co-culture of human microvascular ECs with mouse dorsal root ganglion cells.
- Microarray analysis to identify gene expression changes in ECs.
- In vitro studies on JunB-overexpressing ECs.
- In vivo knockdown of JunB in mouse embryonic limb skin.
Main Results:
- JunB expression was significantly upregulated in ECs following neurovascular interaction.
- Forced JunB expression in ECs promoted tip-like cell formation and angiogenesis in vitro.
- JunB induced expression of vascular endothelial growth factor A (VEGFA) and integrin subunit ITGB3.
- In vivo knockdown of JunB impaired the parallel alignment of blood vessels and nerve fibers.
Conclusions:
- JunB is a critical regulator of embryonic vascular network formation.
- This study provides novel insights into the molecular mechanisms underlying neurovascular interactions during development.
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