Evaluating β-Catenin as a Potential Regulator of Tenogenic Stem Cell Differentiation

Tendons are collagen-rich musculoskeletal tissues that function to anchor muscle to bone, and transfer mechanical force between the two. Unfortunately, tendon injuries are common and tendons have poor self-healing capacity, resulting in long-term dysfunction. There are few treatment options, motivating the need for engineered tendon replacements and regenerative therapies using stem cells. However, there is an incomplete understanding of the biochemical factors and cell signaling pathways that control stem cell differentiation to produce tendon-like tissues (tenogenesis). The overall goal of my research is to better understand the cellular regulators of tenogenesis to advance tissue engineering and regenerative medicine.

To address this goal, my research is focused on exploring what role cell-cell junction proteins and downstream signaling through β-catenin play in regulating tenogenesis. Cells can communicate through cell-cell junction proteins such as cadherins, which physically link cells. β-catenin, an intracellular protein, may anchor cadherins to the actin cytoskeleton, as well as act as a cell signaling protein to regulate cell behavior. The role of β-catenin in tenogenesis has not been well defined. Currently, I am exploring β-catenin’s specific interactions in cadherin-actin coupling and signal transduction in tenogenically differentiating stem cells. These findings will improve our understanding of the cadherin/β-catenin complex in tenogenesis to improve tendon tissue engineering strategies.