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Semaphoring vascular morphogenesis.

Federico Bussolino1, Donatella Valdembri, Francesca Caccavari

  • 1Department of Oncological Sciences and Division of Molecular Angiogenesis, IRCC, Institute for Cancer Research and Treatment, University of Torino School of Medicine, Candiolo, Italy. federico.bussolino@ircc.it

Endothelium : Journal of Endothelial Cell Research
|May 27, 2006
PubMed
Summary
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Semaphorin 3 (SEMA3) proteins guide blood vessel development by regulating endothelial cell interactions with the extracellular matrix. These neural guidance cues are crucial for both forming new blood vessels and remodeling existing ones.

Area of Science:

  • Developmental Biology
  • Cell Biology
  • Vascular Biology

Background:

  • Blood vessel network formation is essential for oxygen and nutrient transport in vertebrate embryos.
  • Endothelial cells (ECs) use integrin-mediated interactions with the extracellular matrix (ECM) during vasculogenesis and angiogenesis.
  • Semaphorins (SEMA), known neural guidance cues, are increasingly recognized for their roles in vascular development.

Purpose of the Study:

  • To investigate the role of class 3 semaphorins (SEMA3) in embryonic blood vessel development.
  • To elucidate the mechanisms by which SEMA3 influences endothelial cell migration, assembly, and vascular remodeling.
  • To understand how SEMA3 signaling affects integrin-ECM interactions.

Main Methods:

  • Analysis of SEMA3 involvement in vasculogenesis and angiogenesis.

Related Experiment Videos

  • Investigation of paracrine and autocrine SEMA3 signaling in ECs.
  • Examination of SEMA3's impact on integrin receptor affinity and downstream signaling pathways.

    • Main Results:

    • Paracrine SEMA3 signaling, alongside vascular endothelial growth factor, regulates EC precursor migration and assembly during vasculogenesis.
    • SEMA3 guides navigating blood vessels through tissue boundaries during sprouting angiogenesis.
    • Autocrine SEMA3 signaling appears to control vascular remodeling via intussusception and fusion.
    • SEMA3 signaling inhibits EC-ECM adhesion by negatively regulating integrin activators R-Ras and talin.

    Conclusions:

    • SEMA3 proteins are critical regulators of vascular network formation and patterning in vertebrates.
    • SEMA3 orchestrates blood vessel development through distinct paracrine and autocrine mechanisms.
    • SEMA3 exerts its vascular effects by modulating integrin-mediated cell-ECM adhesion via plexin receptor signaling.