Loss of cartilage structure, stiffness, and frictional properties in mice lacking PRG4.


OBJECTIVE: To assess the role of the glycoprotein PRG4 in joint lubrication and chondroprotection by measuring friction, stiffness, surface topography, and subsurface histology of the hip joints of Prg4(-/-) and wild-type (WT) mice. METHODS: Friction and elastic modulus were measured in cartilage from the femoral heads of Prg4(-/-) and WT mice ages 2, 4, 10, and 16 weeks using atomic force microscopy, and the surface microstructure was imaged. Histologic sections of each femoral head were stained and graded. RESULTS: Histologic analysis of the joints of Prg4(-/-) mice showed an enlarged, fragmented surface layer of variable thickness with Safranin O-positive formations sometimes present, a roughened underlying articular cartilage surface, and a progressive loss of pericellular proteoglycans. Friction was significantly higher on cartilage of Prg4(-/-) mice at age 16 weeks, but statistically significant differences in friction were not detected at younger ages. The elastic modulus of the cartilage was similar between cartilage surfaces of Prg4(-/-) and WT mice at young ages, but cartilage of WT mice showed increasing stiffness with age, with significantly higher moduli than cartilage of Prg4(-/-) mice at older ages. CONCLUSION: Deletion of the gene Prg4 results in significant structural and biomechanical changes in the articular cartilage with age, some of which are consistent with osteoarthritic degeneration. These findings suggest that PRG4 plays a significant role in preserving normal joint structure and function.





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Publication Info

Coles, Jeffrey M, Ling Zhang, Jason J Blum, Matthew L Warman, Gregory D Jay, Farshid Guilak and Stefan Zauscher (2010). Loss of cartilage structure, stiffness, and frictional properties in mice lacking PRG4. Arthritis Rheum, 62(6). pp. 1666–1674. 10.1002/art.27436 Retrieved from https://hdl.handle.net/10161/15321.

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Stefan Zauscher

Professor in the Thomas Lord Department of Mechanical Engineering and Materials Science

My research lies at the intersection of surface and colloid science, polymer materials engineering, and biointerface science, with four central areas of focus:

  1. Fabrication, manipulation and characterization of stimulus-responsive biomolecular and bio-inspired polymeric nanostructures on surfaces;
  2. Nanotechnology of soft-wet materials and hybrid biological/non-biological microdevices;
  3. Receptor-ligand interactions relevant to the diagnostics of infectious diseases;
  4. Friction of soft-wet materials, specifically the role of glycoproteins on friction in diarthroidal joints.

These four broad lines of inquiry deal with fundamental behaviors of soft-wet materials on surfaces and interfaces. The design and fabrication of these interfaces using "smart" polymeric and biomolecular nanostructures, and the characterization of the resulting structures, are critically important for the development of biomolecular sensors and devices and for bioinspired materials. Key approaches and tools I use in my research are: bottom-up organization on the molecular scale, through self-assembly, in-situ polymerization, and manipulation of intermolecular interactions; topdown fabrication, through scanning probe nanolithography; stimulus-responsive polymers; molecular recognition; and new approaches to sensing and manipulation. This research supports Duke's Pratt School of Engineering strategic initiative to expand research in soft-wet Materials Science.

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