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Updated: Mar 6, 2026

A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors
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RCAN1.4 regulates VEGFR-2 internalisation, cell polarity and migration in human microvascular endothelial cells

Ahmad F Alghanem1,2, Emma L Wilkinson1, Maxine S Emmett1

  • 1MRC Centre for Drug Safety Science, Department of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, Liverpool, L69 3GE, UK.

Angiogenesis
|March 9, 2017
PubMed

Insights

Regulator of calcineurin 1.4 (RCAN1.4) is crucial for endothelial cell migration and vascular development. This study reveals RCAN1.4

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Physiology

Background:

  • Regulator of calcineurin 1 (RCAN1) inhibits the calcineurin pathway.
  • RCAN1 has two isoforms: RCAN1.1 (constitutive) and RCAN1.4 (inducible).
  • RCAN1.4 is upregulated by VEGF in endothelial cells, unlike RCAN1.1.

Purpose of the Study:

  • Investigate the role of RCAN1.4 in endothelial cell function.
  • Determine RCAN1.4's involvement in VEGF signaling and vascular development.
  • Elucidate RCAN1.4's mechanism in endothelial cell migration and polarity.

Main Methods:

  • siRNA-mediated gene silencing of RCAN1.
  • Adenoviral-mediated overexpression of RCAN1.4.
  • Morpholino-based gene silencing in zebrafish.
  • Analysis of VEGFR-2 internalization, cytoskeletal organization, and cell migration.

Main Results:

  • RCAN1.4 regulates agonist-stimulated VEGFR-2 internalization and endothelial cell polarity.
  • RCAN1 is vital for VEGF-mediated cytoskeletal reorganisation, cell migration, and angiogenesis.
  • Overexpression of RCAN1.4 enhances endothelial cell migration.
  • Zebrafish RCAN1.4 orthologue silencing disrupts vascular development.

Conclusions:

  • RCAN1.4 plays a significant role in endothelial cell migration and vascular physiology.
  • RCAN1.4 establishes endothelial cell polarity in response to VEGF, promoting migration.
  • RCAN1.4 is a potential therapeutic target for vascular diseases.
Keywords:
AngiogenesisEndothelialMigrationPolarisationRCAN1VEGFR-2

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