Bonnie Huynh
Pronouns: she/her
Research Mentor(s): Tristan Maerz
Research Mentor School/College/Department: Orthopaedic Surgery / Medicine
Program:
Authors: Bonnie Huynh, Alexander Knights, Easton Farrell, Tristan Maerz
Session: Session 2: 10:00 am – 10:50 am
Poster: 86
Abstract
Inflammation is a key feature of osteoarthritis (OA), and the primary tissue driving this process is the synovium, a soft connective tissue that lines our joints. Inflammation is closely associated with joint pain and stiffening suffered by patients with OA. CD13, a cell surface-bound protein that can take on a soluble form, and its receptor, the Bradykinin receptor B1 (B1R), have both recently been implicated in rheumatoid arthritis. In this study, we explored the roles of CD13 and B1R in joint inflammation using a pre-clinical mouse model of post-traumatic osteoarthritis (PTOA). PTOA was induced in mice via unilateral rupture of the anterior cruciate ligament. This procedure was performed on three genotypes: wild-type, CD13 knockout (KO), and B1R KO mice. 3 days post-injury, in the early inflammatory phase of disease, synovium was harvested from mice of each genotype from both the PTOA knee, and the contralateral (uninjured) knee, which served as a baseline control. We isolated RNA from synovium and performed bulk RNA-sequencing to analyze the transcriptomic signature in each group. Analysis was performed as follows: genes were filtered to eliminate duplicates, sex-linked genes, non protein-coding genes, and zero-read or lowly expressed genes. Two outlier samples were excluded following principal component analysis. We performed differential expression analysis to assess differentially expressed genes (DEGs) in two stages: i) injured vs contralateral synovium within each genotype then ii) overlapping and non-overlapping DEGs between the comparisons for each genotype. Three levels of statistical filtering were employed: padj < 0.05; padj < 0.05 & log2FC > |0.585|; and padj < 0.05 & log2FC > |1|. The DEGs found in each comparison were then compared through the creation of Venn Diagrams. We are now performing pathway analysis to determine what effect deletion of CD13 or B1R has on inflammation and function of synovium in PTOA.
