WISP3 suppresses insulin-like growth factor signaling in human chondrocytes.
Mol Cell Endocrinol
; 279(1-2): 1-8, 2007 Dec 15.
Article
en En
| MEDLINE
| ID: mdl-17942216
WISP3 is essential for maintaining cartilage integrity mainly by regulating the expression of collagen II, and mutations of WISP3 linked to spondyloepiphyseal dysplasia tarda with progressive arthropathy (SEDT-PA) can compromise this function and lead to cartilage loss. The aim of this study was to evaluate the effect of WISP3 on insulin-like growth factor (IGF) signaling in human chondrocytes, investigate whether WISP3 up-regulates collagen II through the IGF signaling pathway, and compare IGF signaling between wild-type and mutant WISP3. Experimental results suggest that WISP3 up-regulates collagen II expression and inhibits the activation of IGF-IR, IRS-1, and ERK kinase in human chondrocytes, and mutation of WISP3 augments IGF signaling in human chondrocytes. In addition to the IGF signaling pathway, WISP3 might up-regulate collagen II expression through an IGF-independent signaling cascade.
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Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Factor I del Crecimiento Similar a la Insulina
/
Transducción de Señal
/
Proteínas de Unión a Factor de Crecimiento Similar a la Insulina
/
Condrocitos
Límite:
Humans
Idioma:
En
Revista:
Mol Cell Endocrinol
Año:
2007
Tipo del documento:
Article