Abstract

Osteoarthritis (OA) is a joint disease that restricts motion and activity, increases risk for other health conditions, and costs the American economy billions of dollars every year. There are currently no disease-modifying treatments available; rather, treatment largely focuses on palliating patients and bridging them to joint replacement surgery. Our work has demonstrated the importance of epigenetic regulation and metabolic alterations in the pathogenesis of OA, specifically through a DNA methyltransferase 3B - 4-aminobutyric acid aminotransferase axis (DNMT3B-ABAT). We targeted this axis with RNA-peptide based nanoparticles and found that either part of the axis could be targeted to successfully mitigate OA pain and tissue changes in a murine injury model. In seeking to better understand the role ABAT plays in OA, we also found that this axis’ effects are partially mediated through the GABAB receptor in articular chondrocytes. This groundbreaking discovery both opens a new avenue for therapeutic investigation, and points to a definition of GABA not merely as a neurotransmitter, but as a small molecule metabolite that sits at the nexus of cellular energetics and cell signaling.

Committee Chair

Regis O'Keefe

Committee Members

Christine Pham; Farshid Guilak; Jie Shen; Marco Colonna

Degree

Doctor of Philosophy (PhD)

Author's Department

Biology & Biomedical Sciences (Molecular Cell Biology)

Author's School

Graduate School of Arts and Sciences

Document Type

Dissertation

Date of Award

3-13-2026

Language

English (en)

Available for download on Saturday, May 06, 2028

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