| Abstract | 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. |
| Authors | Rong-Rong Cui, Jiao Huang, Lu Yi, Hui Xie, Hou-De Zhou, Ling-Qing Yuan, Min Wang, Yi-Qun Peng, Xiang-Hang Luo, Er-Yuan Liao
(Affiliation: Institute of Metabolism and Endocrinology, The Second Xiang-Ya Hospital, Central South University, Changsha, Hunan 410011, PR China.)
|
| Journal | Molecular and cellular endocrinology
(Mol Cell Endocrinol)
Vol. 279
Issue 1-2
Pg. 1-8
(Dec 15 2007)
ISSN: 0303-7207 Ireland |
| PMID | 17942216
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
|
| Chemical References |
- Insulin-Like Growth Factor Binding Proteins
- Recombinant Proteins
- WISP3 protein, human
- Insulin-Like Growth Factor I
- Collagen
- Receptor, IGF Type 1
|
| Topics |
- Cell Line
- Chondrocytes
(drug effects, metabolism)
- Collagen
(metabolism)
- Humans
- Insulin-Like Growth Factor Binding Proteins
(genetics, pharmacology, physiology)
- Insulin-Like Growth Factor I
(drug effects, metabolism)
- Mutation
- Receptor, IGF Type 1
(metabolism)
- Recombinant Proteins
(genetics, pharmacology)
- Signal Transduction
(drug effects, physiology)
- Up-Regulation
(drug effects, genetics)
|
