Integrins and cell signaling in chondrocytes

Issue title: 2nd International Symposium on Mechanobiology: Cartilage and Chondrocyte. Paris, France, April 2001

Article type: Research Article

Authors: Loeser, Richard F.

Affiliations: Departments of Internal Medicine and Biochemistry, Section of Rheumatology, Rush Medical College of Rush‐Presbyterian‐St. Luke's Medical Center, Chicago, IL 60612, USA

Note: [] Address for correspondence: Dr. Richard F. Loeser, MD, Rheumatology, Rush‐Presbyterian‐St. Luke's Medical Center, 1725 W. Harrison, Suite 1017, Chicago, IL 60612, USA. Tel.: +1 312 942 8994; Fax: +1 312 942 3053; E‐mail: [email protected].

Abstract: Integrins are adhesion receptor heterodimers that transmit information from the extracellular matrix (ECM) to the cell through activation of cell signaling pathways. Chondrocytes express several members of the integrin family including α5β1 which is the primary chondrocyte receptor for fibronectin. Cell signaling mediated through integrins regulates several chondrocyte functions including differentiation, matrix remodeling, responses to mechanical stimulation and cell survival. Integrin‐mediated activation of members of the mitogen‐activated protein kinase family likely plays a key role in transmitting signals regulating chondrocyte gene expression. Upstream mediators of mitogen‐activated protein kinase (MAP kinase) activation include focal adhesion kinase (FAK) and proline‐rich tyrosine kinase 2 (pyk2) which are both expressed by chondrocytes. A better understanding of chondrocyte integrin signaling is needed to define the mechanisms by which the ECM regulates chondrocyte function.

Journal: Biorheology, vol. 39, no. 1-2, pp. 119-124, 2002