How TRPV4 damages the blood–neural barrier
Defining TRPV4-mediated cytoskeletal changes that trigger pathological blood-neural barrier disruption
This project looks at how overactive TRPV4 causes the cells lining nerves and the brain to change and leak, which may help people with TRPV4-linked nerve diseases.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Michigan at Ann Arbor NIH-funded |
| Lab location | 1 site (Ann Arbor, United States) |
| Project ID | NIH-11283987 on NIH RePORTER |
What this research studies
This work uses cell cultures, fruit flies, and specially engineered mice that carry TRPV4 mutations to track how overactive TRPV4 changes the scaffolding (actin cytoskeleton) inside blood-vessel cells around nerves and the brain. The team studies calcium-driven signaling and proteins RhoA, CaMKII, and INF2 that appear to link TRPV4 activity to barrier breakdown. They also test whether blocking TRPV4 or these downstream steps prevents blood–neural barrier leakage and subsequent nerve damage in their models. If successful, these experiments could point to drug targets and protection strategies for vulnerable blood–neural barriers.
Who could benefit from this research
Good fit: People with hereditary TRPV4 mutations causing motor neuron disease or neuropathy, or patients with neurological conditions linked to increased TRPV4 activity, are the most relevant future candidates for related trials or sample donation.
Not a fit: Patients whose conditions are unrelated to TRPV4 activity or blood–neural barrier disruption are unlikely to gain direct benefit from this specific work.
Why it matters
Potential benefit: If successful, this work could identify drug targets and approaches to prevent blood–neural barrier breakdown and slow or stop TRPV4-related neurodegeneration.
How similar studies have performed: Prior studies have linked TRPV4 to nerve disease and TRPV4 blockers exist, but the specific pathway connecting TRPV4 to blood–neural barrier breakdown is newly described and not yet proven in people.
Where this research is happening
Ann Arbor, United States
- University of Michigan at Ann Arbor — Ann Arbor, United States (Active)
Researchers
- Principal investigator: Mccray, Brett Andrew — University of Michigan at Ann Arbor
- Study coordinator: Mccray, Brett Andrew
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.