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J. Biol. Chem., Vol. 283, Issue 2, 1043-1051, January 11, 2008

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Cathepsins B, K, and L Are Regulated by a Defined Collagen Type II Peptide via Activation of Classical Protein Kinase C and p38 MAP Kinase in Articular Chondrocytes^*

Anke Ruettger, Susann Schueler, Juergen A. Mollenhauer^¶||, and Bernd Wiederanders¹

From the Institute of Biochemistry I and Orthopaedic Research Unit Eisenberg, Universitätsklinikum, University of Jena, 07743 Jena, Germany, the ^¶Department of Biochemistry, Rush University Medical Center, Chicago, Illinois 60612, and the ^||Natural and Medical Science Institute (NMI) at the University of Tuebingen, 72770 Reutlingen, Germany

Degradation of the extracellular matrix (ECM) is a prominent feature in osteoarthritis (OA), which is mainly because of the imbalance between anabolic and catabolic processes in chondrocytes resulting in cartilage and bone destruction. Various proteases act in concert to degrade matrix components, e.g. type II collagen, MMPs, ADAMTS, and cathepsins. Protease-generated collagen fragments may foster the destructive process. However, the signaling pathways associated with the action of collagen fragments on chondrocytes have not been clearly defined. The present data demonstrate that the N-terminal telopeptide of collagen type II enhances expression of cathepsins B, K, and L in articular chondrocytes at mRNA, protein, and activity levels, mediated at least in part through extracellular calcium. We also demonstrate that the induction is associated with the activation of protein kinase C and p38 MAP kinase.

Received for publication, June 14, 2007 , and in revised form, October 19, 2007.

^* This work was supported in part by European Union Subcontract QLK6-CT-2000-00487, the Deutsche Forschungsgemeinschaft (Grants Mo 980/1-2, Sch 593/1-1, and Ru 1487/1-1), and the Interdisciplinary Centre for Clinical Research (IZKF) Jena. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Tables S1 and S2.

¹ To whom correspondence should be addressed: Inst. of Biochemistry I, Universitätsklinikum, Friedrich-Schiller-Universität, Nonnenplan 2, D-07743 Jena, Germany. Tel.: 49-3641-938611; Fax: 49-3641-938612; E-mail: bwie{at}mti.uni-jena.de.

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