Involvement of the cytoskeletal elements in articular cartilage homeostasis and pathology

• Published in: International journal of experimental pathology 2009-02, Vol.90 (1), p.1-15
• Main Author: Blain, Emma J.
• Format: Article
• Language: English
• Subjects: Actin Cytoskeleton - physiology; actin microfilaments; articular cartilage; Cartilage, Articular - pathology; Cartilage, Articular - physiology; Cartilage, Articular - ultrastructure; chondrocyte; Chondrocytes - ultrastructure; Cytoskeletal Proteins - physiology; cytoskeleton; Cytoskeleton - physiology; Homeostasis - physiology; Humans; Mechanotransduction, Cellular - physiology; Microtubules - physiology; Osteoarthritis - pathology; Osteoarthritis - physiopathology; Review; tubulin microtubules; vimentin intermediate filaments
• ISSN: 0959-9673; 1365-2613
• DOI: 10.1111/j.1365-2613.2008.00625.x

Summary The cytoskeleton of all cells is a three‐dimensional network comprising actin microfilaments, tubulin microtubules and intermediate filaments. Studies in many cell types have indicated roles for these cytoskeletal proteins in many diverse cellular processes including alteration of cell shape, movement of organelles, migration, endocytosis, secretion, cell division and extracellular matrix assembly. The cytoskeletal networks are highly organized in structure enabling them to fulfil their biological functions. This review will primarily focus on the organization and function of the three major cytoskeletal networks in articular cartilage chondrocytes. Articular cartilage is a major load‐bearing tissue of the synovial joint; it is well known that the cytoskeleton acts as a physical interface between the chondrocytes and the extracellular matrix in ‘sensing’ mechanical stimuli. The effect of mechanical load on cytoskeletal element expression and organization will also be reviewed. Abnormal mechanical load is widely believed to be a risk factor for the development of osteoarthritis. Several studies have intimated that the major cytoskeletal networks are disorganized or often absent in osteoarthritic cartilage chondrocytes. The implications and possible reasoning for this are more widely discussed and placed into context with their potential relevance to disease and therapeutic strategies.