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The Amot/integrin protein complex transmits mechanical forces required for vascular expansion
Yuanyuan Zhang1, Yumeng Zhang1, Sumako Kameishi1
1Department of Oncology-Pathology, Bioclinicum, Karolinska Institutet, Stockholm 17164, Sweden.
Cell Reports
|August 25, 2021
Summary
The scaffold protein Angiomotin (Amot) is crucial for vascular development, controlling endothelial cell migration and the formation of new blood vessels. Its absence disrupts blood vessel network expansion by affecting cell movement and force transmission.
Area of Science:
- Cellular biology
- Vascular biology
- Biomechanics
Background:
- Vascular development relies on coordinated cellular activities like migration and differentiation.
- The role of mechanical forces in vascular development is not well understood.
Purpose of the Study:
- To investigate the function of the scaffold protein Angiomotin (Amot) in vascular development.
- To elucidate the mechanisms by which Amot influences endothelial cell behavior and vascular network formation.
Main Methods:
- Utilized an endothelial-specific genetic model in mice.
- Employed in vivo and in vitro molecular approaches.
- Analyzed cell migration, filopodia extension, and protein interactions.
Main Results:
- Deletion of Amot in endothelial cells inhibited vascular network migration and expansion.
- Amot is essential for tip cell migration and filopodia extension.
- Amot directly binds Talin, mediating force transmission from fibronectin to the cytoskeleton.
Conclusions:
- Amot is a key regulator of vascular development, essential for endothelial cell migration and network formation.
- Amot acts as a crucial link in the endothelial integrin adhesome, integrating extracellular matrix cues.
- Amot plays a vital role in mechanotransduction during vascular network assembly.
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