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Assessment of Vascular Regeneration in the CNS Using the Mouse Retina
Published on: June 23, 2014
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Disruption of profilin1 function suppresses developmental and pathological retinal neovascularization.
David Gau1, Lucile Vignaud2, Abigail Allen1
1Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
The Journal of Biological Chemistry
|May 24, 2020
Summary
Profilin1 (PFN1) is crucial for blood vessel formation in the retina. Targeting PFN1 may offer a new treatment strategy for angiogenesis-dependent retinal diseases like diabetic retinopathy.
Area of Science:
- Ophthalmology
- Molecular Biology
- Cell Biology
Background:
- Neovascularization in the eye, particularly in proliferative diabetic retinopathy, can cause vision loss.
- Pathological retinal angiogenesis is a significant cause of blindness.
Purpose of the Study:
- To investigate the role of actin-binding protein PFN1 in retinal angiogenesis.
- To explore PFN1 as a potential therapeutic target for angiogenesis-dependent retinal diseases.
Main Methods:
- Bioinformatics and gene expression analysis of PFN1 in human samples and a murine retinopathy model.
- Conditional knockout mouse models to assess PFN1 function in VECs.
- In vitro and in vivo studies using a small molecule inhibitor targeting PFN1-actin interaction.
Main Results:
- PFN1 expression is elevated in retinal VECs in proliferative diabetic retinopathy and in a murine retinopathy model.
- Deletion of PFN1 in VECs impairs tip cell activity and reduces retinal vascular sprouting.
- PFN1 inhibition reduces VEC motility, proliferation, cord morphogenesis, and pathological neovascularization.
Conclusions:
- PFN1 is essential for actin-based structures and developmental angiogenesis in the retina.
- Targeting the PFN1-actin interaction with small molecules shows promise for treating angiogenesis-dependent retinal diseases.
