Eosinophil Chemotactic Factor‐L (ECF‐L) Enhances Osteoclast Formation by Increasing ICAM‐1 Expression
Identifieur interne : 003350 ( Istex/Curation ); précédent : 003349; suivant : 003351Eosinophil 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.
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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.
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DOI: 10.1196/annals.1346.048
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<term>Eosinophil chemotactic</term>
<term>Ligand</term>
<term>Macrophage protein</term>
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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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