PittsburghV1, Main, Exploration, bibRecord, 00AC53

Eosinophil Chemotactic Factor‐L (ECF‐L) Enhances Osteoclast Formation by Increasing ICAM‐1 Expression

Identifieur interne : 00AC53 ( Main/Exploration ); précédent : 00AC52; suivant : 00AC54

Eosinophil Chemotactic Factor‐L (ECF‐L) Enhances Osteoclast Formation by Increasing ICAM‐1 Expression

Auteurs : Veronica Garcia Palacios [États-Unis] ; Ho Yeon Chung [Corée du Sud] ; Sun Jin Choi [États-Unis] ; Noriyoshi Kurihara [États-Unis] ; Jun Won Lee [États-Unis] ; Lori A. Ehrlich [États-Unis] ; Robert Collins [États-Unis] ; G. David Roodman [États-Unis]

Source :

Annals of the New York Academy of Sciences [ 0077-8923 ] ; 2006-04.

RBID : ISTEX:D7E076DF144F0B346DA2CC8466FC2927DB934388

English descriptors

KwdEn :
- Adhesion, Biol, Cell adhesion molecules, Chem, Chemotactic, Eosinophil, Eosinophil chemotactic, Ligand, Macrophage protein, Mouse marrow cultures, Osteoclast, Osteoclast development, Osteoclast differentiation, Precursor, Rankl, York academy.
Teeft :
- Adhesion, Biol, Cell adhesion molecules, Chem, Chemotactic, Eosinophil, Eosinophil chemotactic, Ligand, Macrophage protein, Mouse marrow cultures, Osteoclast, Osteoclast development, Osteoclast differentiation, Precursor, Rankl, York academy.

Abstract

Abstract: Eosinophil chemotactic factor‐L (ECF‐L) is a novel stimulator of osteoclast (OCL) formation that acts at the differentiation/fusion stage of OCL formation, and is a cofactor for RANK ligand (RANKL). We examined the effects of ECF‐L on the intracellular signaling pathways utilized by RANKL, and on the expression of ICAM‐1/LFA‐1 to determine its mechanism of action. RAW 264.7 and bone marrow cells were treated with RANKL and/or ECF‐L Fc protein to determine their effect on NF‐κB and AP‐1 activity. ECF‐L by itself only modestly increased NF‐κB binding and JNK activity in RAW 264.7 cells, which were further enhanced by RANKL. In contrast, ECF‐L Fc increased LFA‐1α and ICAM‐1 mRNA levels 1.8‐fold in mouse marrow cultures, and anti‐ICAM‐1 almost completely inhibited OCL formation induced by 10−10 M 1,25‐(OH)2D3, and ECF‐L Fc. Furthermore, ECF‐L Fc did not enhance OCL formation by ICAM‐1 knockout (KO) cells. Increased expression of ICAM‐1 by ECF‐L appears to be critical for its effects on OCL formation.

Url:

https://api.istex.fr/document/D7E076DF144F0B346DA2CC8466FC2927DB934388/fulltext/pdf

DOI: 10.1196/annals.1346.048

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Istex, to step Corpus: 003350
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to stream Main, to step Merge: 00B404
to stream Main, to step Curation: 00AC53

Le document en format XML

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<front><div type="abstract">Abstract:  Eosinophil chemotactic factor‐L (ECF‐L) is a novel stimulator of osteoclast (OCL) formation that acts at the differentiation/fusion stage of OCL formation, and is a cofactor for RANK ligand (RANKL). We examined the effects of ECF‐L on the intracellular signaling pathways utilized by RANKL, and on the expression of ICAM‐1/LFA‐1 to determine its mechanism of action. RAW 264.7 and bone marrow cells were treated with RANKL and/or ECF‐L Fc protein to determine their effect on NF‐κB and AP‐1 activity. ECF‐L by itself only modestly increased NF‐κB binding and JNK activity in RAW 264.7 cells, which were further enhanced by RANKL. In contrast, ECF‐L Fc increased LFA‐1α and ICAM‐1 mRNA levels 1.8‐fold in mouse marrow cultures, and anti‐ICAM‐1 almost completely inhibited OCL formation induced by 10−10 M 1,25‐(OH)2D3, and ECF‐L Fc. Furthermore, ECF‐L Fc did not enhance OCL formation by ICAM‐1 knockout (KO) cells. Increased expression of ICAM‐1 by ECF‐L appears to be critical for its effects on OCL formation.</div>
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Eosinophil Chemotactic Factor‐L (ECF‐L) Enhances Osteoclast Formation by Increasing ICAM‐1 Expression

Eosinophil Chemotactic Factor‐L (ECF‐L) Enhances Osteoclast Formation by Increasing ICAM‐1 Expression

Source :

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

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