Liam Cotter
Pronouns: He/Him
Research Mentor(s): Tristan Maerz
Co-Presenter:
Research Mentor School/College/Department: Orthopaedic Surgery / Medicine
Presentation Date: April 20
Presentation Type: Poster
Session: Session 3 – 1:40pm – 2:30 pm
Room: League Ballroom
Authors: Liam Cotter, Alexander Knights, Tristan Maerz
Presenter: 111
Abstract
While little is known of the role of Wnt signaling in the development of osteoarthritis, research in other contexts such as cancer and bone formation suggests its involvement in the onset of inflammation and fibrosis. As these phenomena are also involved in osteoarthritis, determining what activates Wnt signaling and how it is associated with the cellular processes responsible for inflammation and fibrosis will provide new insights into the mechanisms of the disease. In this study, cells known as fibroblast-like synoviocytes (FLS) were isolated from mouse paws and exposed to six treatments: PBS (vehicle), R-spondin 2, Wnt3a, a combination of Wnt3a and R-spondin 2, DMOG, and TGF-ß1. The R-spondin 2 and Wnt3a treatments were expected to activate the Wnt signaling pathway while the DMOG and TGF-ß1 treatments were expected to activate fibrosis. After a 96-hour treatment, the FLS were harvested for gene expression analysis via qPCR. The genes targeted for qPCR are known to be associated with Wnt signaling (Axin2 and Lef1), inflammation (IL6), and fibrosis (aSMA and Col3a1). According to the results, extended exposure of the FLS to treatments known to activate Wnt signaling produced changes in the expression of genes associated with Wnt signaling, inflammation, and fibrosis. These findings may illuminate the role of Wnt signaling in fibrotic and inflammatory activity in FLS and supply the background knowledge necessary for the development of new treatments for osteoarthritis.
Biomedical Sciences, Interdisciplinary
