F2L, a peptide derived from heme-binding protein, inhibits LL-37-induced cell proliferation and tube formation in human umbilical vein endothelial cells.
Lee. Sun Young SY; Lee. Mi-Sook MS; Lee. Ha Young HY; Kim. Sang Doo SD; Shim. Jae Woong JW; Jo. Seong Ho SH; Lee. Jae Won JW; Kim. Joon Youn JY; Choi. Young-Whan YW; Baek. Suk-Hwan SH; Ryu. Sung Ho SH; Bae. Yoe-Sik YS
Key Findings
- F2L binds to the FPRL1 receptor and blocks its activity in endothelial cells
- LL‑37 normally triggers cell proliferation and tube formation, which are steps in new blood‑vessel growth
- F2L inhibits the LL‑37‑driven proliferation and tube formation despite stimulating cell migration
Practical Outcomes
- For now, this research is purely cellular and doesn’t translate into a usable supplement or protocol. It suggests that targeting the LL‑37/FPRL1 pathway might one day help manage vascular health or diseases with excess blood‑vessel growth, but no dosage or safety data exist for personal use yet.
Summary
Researchers found that a small protein called F2L can stop another molecule, LL‑37, from making blood‑vessel cells grow and form new vessels in lab dishes. While F2L itself makes the cells move a bit, it blocks the growth‑promoting signals of LL‑37, hinting it could be useful for controlling unwanted blood‑vessel formation.
Abstract
F2L, a peptide derived from heme-binding protein, was originally identified as an endogenous ligand for formyl peptide receptor-like (FPRL)2. Previously, we reported that F2L inhibits FPR and FPRL1-mediated signaling in neutrophils. Since endothelial cells express functional FPRL1, we examined the effect of F2L on LL-37 (an FPRL1 agonist)-induced signaling in human umbilical vein endothelial cells (HUVECs). F2L stimulated the chemotactic migration in HUVECs. However, F2L inhibited FPRL1 activity, resulting in the inhibition of cell proliferation and tube formation induced by LL-37 in HUVECs. We suggest that F2L will potentially be useful in the study of FPRL1 signaling and the development of drugs to treat diseases involving the FPRL1 in the vascular system.
Study Information
pubmed
2007
2007-12-18T00:00:00.000Z
10.1016/j.febslet.2007.12.015
18
34