How a retinal protein (Bim) affects blood-vessel damage in oxygen-related infant eye disease
Neural Retina-Specific Bim Expression and Hyperoxia Sensitivity of the Developing Retinal Vasculature
Researchers are looking at whether a protein called Bim in retinal nerve cells makes the developing eye blood vessels of premature infants more likely to be damaged by high oxygen levels that cause retinopathy of prematurity.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Wisconsin-Madison NIH-funded |
| Lab location | 1 site (Madison, United States) |
| Project ID | NIH-11136981 on NIH RePORTER |
What this research studies
From a patient's perspective, the team uses a well-established mouse model that mimics retinopathy of prematurity to reproduce oxygen-related blood-vessel damage in the retina. They remove or reduce the Bim protein in specific retinal cell types, focusing on inner retinal neurons, and compare how the blood vessels respond to high-oxygen exposure. The researchers will measure vessel loss, abnormal new vessel growth, and levels of growth factors like VEGF to see how neuronal Bim controls vascular behavior. Results will help clarify whether targeting neuronal Bim could protect the developing retina from oxygen-induced injury.
Who could benefit from this research
Good fit: This research is most relevant to families of premature infants at risk for retinopathy of prematurity and to patients interested in future treatment options aimed at protecting developing retinal blood vessels.
Not a fit: Patients with unrelated eye conditions or adults without developing-retina concerns are unlikely to gain direct benefit from this specific preclinical work.
Why it matters
Potential benefit: If successful, this work could point to new ways to prevent or reduce blood-vessel damage in babies at risk for retinopathy of prematurity.
How similar studies have performed: Prior mouse studies showed that removing Bim globally protects against oxygen-induced retinal vessel loss while deleting Bim in endothelial cells, pericytes, or astrocytes did not, so this project builds on those findings by focusing on neuronal Bim.
Where this research is happening
Madison, United States
- University of Wisconsin-Madison — Madison, United States (Active)
Researchers
- Principal investigator: Zaitoun, Ismail S — University of Wisconsin-Madison
- Study coordinator: Zaitoun, Ismail S
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page below.