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Updated: Jul 12, 2026

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Published on: November 23, 2014
Opioid growth factor modulates angiogenesis
J Blebea1, J E Mazo, T K Kihara
1Department of Surgery and the Department of Neuroscience and Anatomy, The Pennsylvania State University College of Medicine, Hershey, PA, USA.
Endogenous opioids, specifically opioid growth factor (OGF), inhibit angiogenesis in vivo. Blocking OGF with naltrexone promotes blood vessel growth, suggesting a therapeutic target for vascular diseases.
Area of Science:
- Molecular Biology
- Vascular Biology
- Endocrinology
Background:
- Induced angiogenesis is a therapeutic strategy for occlusive arterial atherosclerotic disease.
- The role of endogenous opioids in modulating angiogenesis remains largely unexplored.
Purpose of the Study:
- To investigate the potential role of endogenous opioids in regulating angiogenesis.
- To determine if opioid growth factor (OGF) influences blood vessel formation in vivo.
Main Methods:
- Utilized the chick chorioallantoic membrane (CAM) as an in vivo model for angiogenesis.
- Applied OGF, opioid receptor antagonists (naloxone, naltrexone), retinoic acid, and vascular endothelial growth factor (VEGF) to CAMs.
- Quantified blood vessel number and length using digital imaging and performed immunocytochemistry for OGF and its receptor (OGFr).
Main Results:
- Opioid growth factor significantly inhibited angiogenesis, reducing blood vessel number and length by 35% and 20%, respectively.
- Naltrexone, an opioid antagonist, significantly increased blood vessel number and length by 51% and 24%, indicating receptor-mediated effects.
- OGF and OGFr were detected in endothelial and mesenchymal cells of the CAM vasculature.
Conclusions:
- Endogenous opioids, particularly OGF, play a significant role in modulating in vivo angiogenesis.
- OGF acts as a tonically active peptide regulating angiogenesis through receptor-mediated mechanisms.
- These findings highlight a novel pathway for therapeutic intervention in vascular diseases.
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