PUBLICATION

OPN3-mediated positive regulation of angiogenesis in HUVECs through VEGFR2 interaction

Authors
Luo, H., Zhang, W., Zeng, W., Wang, Y., Feng, J., Lan, Y., Dong, X., Liu, T., Sun, Y., Lu, H.
ID
ZDB-PUB-250401-27
Date
2025
Source
Communications biology   8: 529529 (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • Signal Transduction
  • Vascular Endothelial Growth Factor Receptor-2*/genetics
  • Vascular Endothelial Growth Factor Receptor-2*/metabolism
  • Cell Proliferation
  • Human Umbilical Vein Endothelial Cells*/metabolism
  • Zebrafish*
  • Rod Opsins/genetics
  • Rod Opsins/metabolism
  • Cell Movement
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
  • Animals
  • Humans
  • Neovascularization, Physiologic*
  • Angiogenesis
PubMed
40164822 Full text @ Commun Biol
Abstract
Many rhodopsin-like G-protein-coupled receptors (Rh-GPCRs) are known to either promote or inhibit angiogenesis. Among these, Opsin 4 and Opsin 5 are specifically involved in vascular development within the eye. Opsin 3 (OPN3), another member of Rh-GPCRs, performs a variety of light-dependent and light-independent functions in extraocular tissue. However, its role in endothelial cells and angiogenesis remains unclear. Here, we found that OPN3 knockdown or knockout in zebrafish impairs embryonic angiogenesis and vascular development. Similarly, silencing OPN3 in human umbilical vein endothelial cells (HUVECs) inhibits cellular proliferation, migration, sprouting, and tube formation, while OPN3 overexpression promotes these cellular processes. Moreover, OPN3 regulates angiogenesis in HUVECs through the VEGFR2-AKT pathway, with OPN3 and VEGFR2 co-localizing at the plasma membrane and forming a physical complex. These findings provide new insights into the non-light-dependent functions of OPN3 in angiogenesis, expanding our understanding of its physiological roles and offering potential therapeutic strategies for angiogenesis-related diseases.
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