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F2L, a peptide derived from heme‐binding protein, inhibits LL‐37‐induced cell proliferation and tube formation in human umbilical vein endothelial cells
Author(s) -
Lee Sun Young,
Lee Mi-Sook,
Lee Ha Young,
Kim Sang Doo,
Shim Jae Woong,
Jo Seong Ho,
Lee Jae Won,
Kim Joon Youn,
Choi Young-Whan,
Baek Suk-Hwan,
Ryu Sung Ho,
Bae Yoe-Sik
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.12.015
Subject(s) - umbilical vein , chemotaxis , microbiology and biotechnology , formyl peptide receptor , heme , human umbilical vein endothelial cell , endothelial stem cell , receptor , peptide , agonist , endogeny , biology , chemistry , biochemistry , in vitro , enzyme
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.