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Complex Formation between VEGFR2 and the β2-Adrenoceptor.

Laura E Kilpatrick1, Diana C Alcobia2, Carl W White3

  • 1Division of Physiology, Pharmacology & Neuroscience, School of Life Sciences, University of Nottingham, Nottingham NG7 2UH, UK; Centre of Membrane Proteins and Receptors, University of Birmingham and University of Nottingham, The Midlands, UK.

Cell Chemical Biology
|April 9, 2019
PubMed
Summary
This summary is machine-generated.

Vascular endothelial growth factor receptor 2 (VEGFR2) and beta-2 adrenoceptors form complexes that influence signaling. This interaction may explain how propranolol treats infantile hemangioma.

Keywords:
BRETCRISPR/Cas9NanoBRETVEGFR2infantile haemangiomareceptor oligomerisationβ(2)-adrenoceptorsβ-arrestin

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Area of Science:

  • Molecular biology
  • Cellular signaling
  • Pharmacology

Background:

  • Vascular endothelial growth factor (VEGF) and its receptor VEGFR2 are key in angiogenesis.
  • Infantile hemangioma involves excessive vascular endothelial cell proliferation.
  • Propranolol is the primary treatment for infantile hemangioma, but its mechanism is unclear.

Purpose of the Study:

  • To investigate the molecular interactions between VEGFR2 and the beta-2 adrenoceptor.
  • To elucidate the mechanism of propranolol's action in infantile hemangioma.

Main Methods:

  • Bioluminescence resonance energy transfer (BRET) was used.
  • VEGFR2 was genetically tagged with NanoLuc luciferase.

Main Results:

  • Oligomeric complexes of VEGFR2 and beta-2 adrenoceptor formed in cell membranes and endosomes.
  • These complexes were induced by agonist treatment and coupled to signaling proteins.
  • VEGFR2 activation prolonged beta-2 adrenoceptor-beta-arrestin2 coupling.

Conclusions:

  • Protein-protein interactions between VEGFR2, beta-2 adrenoceptor, and beta-arrestin2 are identified.
  • These interactions offer insights into infantile hemangioma pathogenesis and propranolol's therapeutic effects.