Age-dependent alteration of TGF-β signalling in osteoarthritis

被引：163

作者：

van der Kraan, Peter M. ^{[1
]}

Goumans, Marie-Jose ^{[2
,3
]}

Davidson, Esmeralda Blaney ^{[1
]}

ten Dijke, Peter ^{[2
,3
]}

机构：

[1] Radboud Univ Nijmegen, Med Ctr Nijmegen, Dept Rheumatol, NL-6525 GA Nijmegen, Netherlands

[2] Leiden Univ, Med Ctr, Dept Mol Cell Biol, NL-2300 RC Leiden, Netherlands

[3] Leiden Univ, Med Ctr, Ctr Biomed Genet, NL-2300 RC Leiden, Netherlands

来源：

CELL AND TISSUE RESEARCH | 2012年 / 347卷 / 01期

关键词：

Aging; Bone morphogenetic protein; Osteoarthritis; Osteophyte; Signalling; Smad; Transforming growth factor-beta; MURINE KNEE-JOINT; ACID REPEAT POLYMORPHISM; OSTEOPHYTE FORMATION; ARTICULAR-CARTILAGE; TRANSFORMING GROWTH-FACTOR-BETA-1; CHONDROCYTE DIFFERENTIATION; ENDOCHONDRAL OSSIFICATION; BONE-DEVELOPMENT; ORGAN-CULTURE; ASPORIN GENE;

D O I：

10.1007/s00441-011-1194-6

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

Osteoarthritis (OA) is a disease of articular cartilage, with aging as the main risk factor. In OA, changes in chondrocytes lead to the autolytic destruction of cartilage. Transforming growth factor-beta has recently been demonstrated to signal not only via activin receptor-like kinase 5 (ALK5)-induced Smad2/3 phosphorylation, but also via ALK1-induced Smad1/5/8 phosphorylation in articular cartilage. In aging cartilage and experimental OA, the ratio ALK1/ALK5 has been found to be increased, and the expression of ALK1 is correlated with matrix metalloproteinase-13 expression. The age-dependent shift towards Smad1/5/8 signalling might trigger the differentiation of articular chondrocytes with an autolytic phenotype.

引用

页码：257 / 265

页数：9

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