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rdf:type |
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|
lifeskim:mentions |
|
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pubmed:issue |
2
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pubmed:dateCreated |
2008-1-18
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pubmed:abstractText |
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.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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|
pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0014-5793
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pubmed:author |
pubmed-author:BaeYoe-SikYS,
pubmed-author:BaekSuk-HwanSH,
pubmed-author:ChoiYoung-WhanYW,
pubmed-author:JoSeong HoSH,
pubmed-author:KimJoon YounJY,
pubmed-author:KimSang DooSD,
pubmed-author:LeeHa YoungHY,
pubmed-author:LeeJae WonJW,
pubmed-author:LeeMi-SookMS,
pubmed-author:LeeSun YoungSY,
pubmed-author:RyuSung HoSH,
pubmed-author:ShimJae WoongJW
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pubmed:issnType |
Print
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pubmed:day |
23
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pubmed:volume |
582
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
273-8
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pubmed:meshHeading |
|
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pubmed:year |
2008
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pubmed:articleTitle |
F2L, a peptide derived from heme-binding protein, inhibits LL-37-induced cell proliferation and tube formation in human umbilical vein endothelial cells.
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pubmed:affiliation |
Department of Biochemistry, College of Medicine, Dong-A University, Busan, Republic of Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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