Biology and Pathology of Bone and Joint: Molecular Targets For an Effective Therapy

Session Type: ACR Abstract Submissions
Tuesday, November 8, 2011: 2:30 PM-4:00 PM
W193a (McCormick Place West)
Moderators: Mary Goldring, PhD, Hospital for Special Surgery/Weill Cornell Med Col and Martin K. Lotz, MD, Scripps Rsch Inst
2:30 PM
Compromised Expression of the Complement Membrane Inhibitor CD59a Propagates Age-Related Joint Degeneration in Mice 
Vishal Paringe1, Anja C. Bloom1, Ernest Choy1, Bryan P. Morgan1 and Anwen S. Williams2, 1Cardiff University, Cardiff, ENGLAND, United Kingdom, 2Cardiff University, Cardiff, United Kingdom
2:45 PM
F-Spondin (spondin-1) Null Mice Exhibit Increased Bone Formation
Mukundan Attur1, Glyn Palmer1, James Liu1, Yang Qing2, Daniel Rifkin2, Frank Beier3 and Steven B. Abramson1, 1NYU Hospital for Joint Diseases, New York, NY, 2New York University School of Medicine, New York, NY, 3Schulich School of Medicine and Dentistry, London, ON
3:00 PM
Synovial Wnt and Wnt-1-Induced Secreted Protein 1 Expression Induce Osteoarthritis-Like Cartilage Damage by Skewing of Transforming Growth Factor-Beta Signaling From Smad 2/3 towards Smad 1/5/8 Phosphorylation
Martijn H. van den Bosch, Arjen B. Blom, Peter L. van Lent, Henk M. van Beuningen, Fons A. van de Loo, Esmeralda N. Blaney Davidson, Peter M. van der Kraan and Wim B. van den Berg, Radboud University Nijmegen Medical Centre, Nijmegen, Netherlands
3:15 PM
Inhibition of Osteoclast Formation by Adenosine A2A Receptor Is Due to Inhibition of NFkB Nuclear Translocation by a PKA-Mediated Mechanism
Aranzazu Mediero, NYU School of Medicine, New York, NY and Bruce N. Cronstein, New York Univ Medical Center, New York, NY
3:30 PM
MicroRNA-453 Modulates Sonic Hedgehog Gene Expression in Human Chondrocytes by Directly Targeting Its Open Reading Frame
Nahid Akhtar, Case Western Reserve University/Metrohealth Medical Center, Cleveland, OH and Tariq M. Haqqi, Metro Health Medical Center/Case Western Reserve University, Cleveland, OH
3:45 PM
The Unfolded Protein Response (UPR) Is Activated by Biomechanical Stress in Normal Cartilage Chondrocytes, but Priming of the UPR Prior to Mechanical Stress Results in Increased Cartilage Catabolism
Matthew R. Husa1, Freyr Petturson1, Ron June1, Shawn Grogan2, Darryl D'Lima2, Martin K. Lotz2, Ru Liu-Bryan1 and Robert Terkeltaub1, 1UCSD/VAMC, La Jolla, CA, 2The Scripps Research Institute, La Jolla, CA
See more of: ACR Abstract Submissions

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