F2L, a peptide derived from heme-binding protein, inhibits LL-37-induced cell proliferation and tube formation in human umbilical vein endothelial cells

被引：21

作者：

Lee, Sun Young ^{[1
]}

Lee, Mi-Sook ^{[2
]}

Lee, Ha Young ^{[1
]}

Kim, Sang Doo ^{[1
]}

Shim, Jae Woong ^{[1
]}

Jo, Seong Ho ^{[1
]}

Lee, Jae Won ^{[3
]}

Kim, Joon Youn ^{[3
]}

Choi, Young-Whan ^{[4
]}

Baek, Suk-Hwan ^{[5
]}

Ryu, Sung Ho ^{[2
]}

Bae, Yoe-Sik ^{[1
]}

机构：

[1] Dong A Univ, Coll Med, Dept Biochem, Pusan 602714, South Korea

[2] Pohang Univ Sci & Technol, Div Mol & Life Sci, Pohang 790784, South Korea

[3] Dong A Univ, Coll Med, Dept Prevent Med, Pusan 602714, South Korea

[4] Pusan Natl Univ, Coll Nat Resources & Life Sci, Dept Hort Biosci, Miryang 627706, South Korea

[5] Yeungnam Univ, Coll Med, Dept Biochem & Mol Biol, Taegu 705717, South Korea

来源：

FEBS LETTERS | 2008年 / 582卷 / 02期

关键词：

F2L; formyl peptide receptor-like 1; chemotaxis; angiogenesis; cell proliferation; endothelial cell;

D O I：

10.1016/j.febslet.2007.12.015

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 [生物化学与分子生物学]; 081704 [应用化学];

摘要：

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. (C) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：273 / 278

页数：6

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