Neutrophil-derived cathelicidin protects from neointimal hyperplasia.
Soehnlein. Oliver O; Wantha. Sarawuth S; Simsekyilmaz. Sakine S; Döring. Yvonne Y; Megens. Remco T A RT; Mause. Sebastian F SF; Drechsler. Maik M; Smeets. Ralf R; Weinandy. Stefan S; Schreiber. Fabian F; Gries. Thomas T; Jockenhoevel. Stefan S; Möller. Martin M; Vijayan. Santosh S; van Zandvoort. Marc A M J MA; Agerberth. Birgitta B; Pham. Christine T CT; Gallo. Richard L RL; Hackeng. Tilman M TM; Liehn. Elisa A EA; Zernecke. Alma A; Klee. Doris D; Weber. Christian C
Key Findings
- Neutrophil‑derived LL‑37 promotes re‑endothelialization (the regrowth of the inner lining of blood vessels).
- Enhanced re‑endothelialization leads to less neointimal hyperplasia (the tissue growth that causes in‑stent stenosis).
- A miniaturized Nitinol stent coated with LL‑37 reduced in‑stent narrowing in a mouse model of atherosclerosis.
Practical Outcomes
- For most biohackers, the study is not directly actionable because it involves a specialized, implanted stent coating, which isn’t something you can self‑administer. However, it suggests that LL‑37 may have vascular‑healing properties, hinting that future therapies or supplements could target this pathway. Keep an eye on clinical trials before considering any off‑label use.
Summary
Researchers found that the natural peptide LL‑37, which is released by neutrophils, helps blood vessels heal faster after a stent is placed, cutting down the thickening that can block the artery again. In mice, a tiny stent coated with LL‑37 reduced this re‑narrowing, showing the peptide’s potential to improve vascular recovery.
Abstract
Percutaneous transluminal angioplasty with stent implantation is used to dilate arteries narrowed by atherosclerotic plaques and to revascularize coronary arteries occluded by atherothrombosis in myocardial infarction. Commonly applied drug-eluting stents release antiproliferative or anti-inflammatory agents to reduce the incidence of in-stent stenosis. However, these stents may still lead to in-stent stenosis; they also show increased rates of late stent thrombosis, an obstacle to optimal revascularization possibly related to endothelial recovery. Here, we examined the contribution of neutrophils and neutrophilic granule proteins to arterial healing after injury. We found that neutrophil-borne cathelicidin (mouse CRAMP, human LL-37) promoted reendothelization and thereby limited neointima formation after stent implantation. We then translated these findings to an animal model using a neutrophil-instructing, biofunctionalized, miniaturized Nitinol stent coated with LL-37. This stent reduced in-stent stenosis in a mouse model of atherosclerosis, suggesting that LL-37 may promote vascular healing after interventional therapy.
Study Information
pubmed
2011
2011-10-05T00:00:00.000Z
10.1126/scitranslmed.3002531
121
53