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Journal of Undergraduate Research

Keywords

osteoarthritis, Dmm, disproportionate micromelia mutation, mice, type IIA procollagen

College

Life Sciences

Department

Physiology and Developmental Biology

Abstract

Arthritis is a painful, debilitating disease that affects sixty-six million Americans (The Arthritis Foundation 2005). Osteoarthritis (OA), results in joint degeneration caused by cartilage erosion and synovial inflammation. While the causes of OA remain unclear, current evidence suggests that both mechanical and biochemical factors can initiate OA. Ethical and practical issues limiting the availability of human tissue in OA research necessitate the use of animal models. Mice with the disproportionate micromelia mutation (Dmm) exhibit histological characteristics similar to those of humans with OA. Use of Dmm as a model of OA may lead a discovery of a common mechanism associated with human OA Within our study, we tested parameters to further validate the Dmm mouse as a viable model for human OA. We assayed the presence of type IIA procollagen (Col2a1), a proposed biomarker of human OA, in both wild-type and mutant mouse knee joint articular cartilage at specific age intervals. We hypothesized that Dmm mice would have more intense staining than that of the mutant mice, a result of Dmm’s early OA onset. This then would lead to the conclusion that Col2a1 gene product is up-regulated and thus a similar biomarker for humans and mouse OA. Further, we expected mutant staining to peak around three to six months with onset of OA, and to diminish around nine or twelve months following deterioration of the cartilage

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