Alejandra Abramson
Research Mentor(s): Ligia Buloto Schmitd
Mentor Department: Cell and Developmental Biology
Authors: Alejandra Abramson, Ligia Buloto Schmitd, Roman Giger
Session: Session 1 (9:00am – 9:50am)
Presentation Type: Oral
Abstract
Schwann cells (SCs) play a crucial role in nerve regeneration following injury by transitioning into a repair-promoting state that facilitates axonal regrowth and remyelination. Sonic Hedgehog (SHH) signaling has been implicated in various cellular processes, including development and tissue repair. Shortly after an injury, SCs reprogram into a repair state, marked by the expression of c-Jun (Jun gene) and p75 (Ngfr gene). SHH is also expressed in SCs exclusively after nerve injury, but its role in SC function during nerve regeneration remains unclear. Understanding the molecular mechanisms governing SC behavior could provide insights into optimizing nerve repair strategies. In this study, we cultured primary SCs from sciatic nerves from wild-type mice on a C57BL6/J genetic background and examined SHH’s effects on the repair phenotype of SCs. Our main goal was determining whether SHH influences their ability to maintain a repair-promoting state. Cells were cultured using optimized protocols for SC isolation, treated with a hedgehog pathway inhibitor or vehicle, and investigated for the repair markers c-Jun and P75, indicative of the repair phenotype. Preliminary results suggest that SHH does not directly affect SC capacity to remain in the repair state. Future in vitro experiments will involve treating primary SC cultures with SHH ligands. However, it is possible that the role of SHH in nerve regeneration involves paracrine signaling to other cells to regulate broader aspects of tissue recovery. Further investigations are necessary to explore this possibility. For that, we are generating genetically modified mouse models where Schwann cells and mesenchymal cells will lack hedgehog signaling. Nerve regeneration studies will be conducted in these mice. Optimizing nerve regeneration is critical for improving recovery outcomes following peripheral nerve injuries. By identifying key molecular regulators of SC behavior, we aim to refine therapeutic approaches that enhance repair efficiency. Future studies will clarify SHH’s indirect roles in nerve repair and potential applications in regenerative medicine.
