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Published on: May 20, 2011

Class 3 semaphorins control vascular morphogenesis by inhibiting integrin function.

Guido Serini¹, Donatella Valdembri, Sara Zanivan

¹Division of Molecular Angiogenesis, IRCC, Institute for Cancer Research and Treatment, and Department of Oncological Sciences, University of Torino School of Medicine, 10060 Candiolo, TO, Italy. guido.serini@ircc.it

|July 25, 2003

Summary

This summary is machine-generated.

Endothelial cells use semaphorins 3 (SEMA3) to control integrin activation, enabling vascular plasticity during development and angiogenesis. This finding reveals SEMA3 as a key regulator of cell adhesion and migration in blood vessel formation.

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Area of Science:

Cell Biology
Developmental Biology
Vascular Biology

Background:

Endothelial cell motility and morphogenesis are crucial for vascular remodelling, regulated by integrin adhesion receptors.
Dynamic cell adhesion is necessary for endothelial cells to respond to extracellular matrix cues during angiogenesis.

Purpose of the Study:

To investigate the role of class 3 semaphorins (SEMA3) in regulating endothelial cell integrin function and vascular development.
To determine if endothelial cells produce autocrine signals that modulate integrin-mediated adhesion and migration.

Main Methods:

Studied endothelial cells during vascular development and experimental angiogenesis.
Investigated the effects of disrupting endogenous SEMA3 function and applying exogenous SEMA3 proteins.
Utilized dominant-negative SEMA3 receptor misexpression in chick embryo endothelial cells.
Examined vascular defects in Sema3a null mice.

Main Results:

Endothelial cells generate autocrine SEMA3 signals that localize to adhesive sites.
Disrupting SEMA3 function enhances integrin-mediated adhesion and migration.
Exogenous SEMA3 proteins inhibit integrin activation.
Impaired SEMA3 signaling leads to hyperactive integrins and defective vascular remodelling.

Conclusions:

Endothelial SEMA3 proteins act as negative regulators of integrin activation.
SEMA3 proteins provide vascular plasticity by controlling integrin function during angiogenesis.
These findings highlight SEMA3 signaling as a critical mechanism for vascular development and remodelling.