Stopping neutrophils from sticking during inflammation and blood-flow injury
Molecular regulation of β2 integrin activation in neutrophil adhesion and inflammation
This project looks at whether blocking a protein called kindlin-3 that helps white blood cells stick to vessel walls can lower inflammation and tissue damage after heart attacks and similar blood-flow injuries.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Nevada Reno NIH-funded |
| Lab location | 1 site (Reno, United States) |
| Project ID | NIH-11133004 on NIH RePORTER |
What this research studies
Researchers will use genetically engineered reporter mice to watch how neutrophils turn on β2 integrins and how the proteins kindlin-3 and talin-1 behave during inflammation. They will image these molecules in real time and probe the molecular steps that allow neutrophils to arrest on blood vessel walls. The team will test whether disrupting kindlin-3–dependent activation of β2 integrins reduces inflammatory damage in models of ischemia-reperfusion injury. Findings aim to reveal targets that could be used to design therapies to limit damaging inflammation after heart attacks or other blood-flow injuries.
Who could benefit from this research
Good fit: People with or at high risk for cardiovascular events or ischemia-reperfusion injury (for example those who have had heart attacks, strokes, or certain surgeries) are the groups most likely to benefit from treatments based on these findings.
Not a fit: Patients whose conditions are not driven by neutrophil-mediated inflammation or who have unrelated non-inflammatory disorders are unlikely to benefit directly from this specific line of work.
Why it matters
Potential benefit: If successful, this work could point to new ways to reduce inflammation and preserve tissue after heart attacks, strokes, or surgery-related blood-flow injuries.
How similar studies have performed: Other animal studies targeting neutrophil adhesion and integrin function have shown promise in reducing inflammation, but targeting kindlin-3 specifically is a newer, less-tested approach.
Where this research is happening
Reno, United States
- University of Nevada Reno — Reno, United States (Active)
Researchers
- Principal investigator: Wen, Lai — University of Nevada Reno
- Study coordinator: Wen, Lai
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.