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Updated: Mar 12, 2026

Real-time Imaging of Endothelial Cell-cell Junctions During Neutrophil Transmigration Under Physiological Flow
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Sema3d controls collective endothelial cell migration by distinct mechanisms via Nrp1 and PlxnD1

Mailin Julia Hamm1,2, Bettina Carmen Kirchmaier3,4, Wiebke Herzog5,2

  • 1Cells-in-Motion Cluster of Excellence, University of Muenster, 48149 Muenster, Germany.

The Journal of Cell Biology
|November 2, 2016
PubMed

Insights

Sema3d guides blood vessel development in zebrafish through two pathways: mesenchymal repulsion and endothelial cell self-signaling. This research clarifies mechanisms of endothelial cell migration and cardiovascular development.

Area of Science:

  • Cardiovascular Biology
  • Cell Migration
  • Developmental Biology

Background:

  • Endothelial cell (EC) migration is crucial for cardiovascular development, requiring precise molecular regulation.
  • Class III Semaphorins, known for neuronal guidance, are implicated in cardiovascular development, with SEMA3D disruptions linked to defects.
  • Mechanisms of Semaphorin 3D (Sema3d) in cardiovascular development remain unclear.

Purpose of the Study:

  • To elucidate the mechanisms by which Sema3d regulates collective endothelial cell migration during zebrafish cardiovascular development.
  • To identify the specific signaling pathways and cellular processes involved in Sema3d-mediated EC migration.

Main Methods:

  • Utilized zebrafish as a model organism to study cardiovascular development in vivo.
  • Investigated Sema3d signaling pathways involving PlexinD1 and Neuropilin1.
  • Analyzed the regulation of the actin cytoskeleton and cell morphology in response to Sema3d signaling.

Main Results:

  • Demonstrated that mesenchymal Sema3d repels and guides common cardinal vein outgrowth via PlexinD1 signaling.
  • Identified a novel autocrine function of Sema3d in ECs, regulating actin network organization and morphology.
  • Showed that autocrine Sema3d signaling acts through Neuropilin1, RhoA, and Rock to stabilize the endothelial sheet.

Conclusions:

  • Sema3d employs dual mechanisms to regulate collective EC migration: mesenchymal repulsion and autocrine signaling within ECs.
  • These findings reveal new insights into Sema3d's role in cardiovascular development and collective cell migration.
  • The study highlights the importance of understanding Sema3d signaling for both normal development and potential therapeutic interventions.

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