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Document Type
Poster
Publication Date
10-1-2025
Abstract
Vocal fold scarring (VFS), a fibrotic condition of the lamina propria, commonly results from prolonged intubation or laryngeal trauma and leads to impaired vocal function and often irreversible dysphonia. Following injury, fibroblasts are activated by proinflammatory cytokines—particularly transforming growth factor beta 1 (TGFβ1)—which induces their differentiation into contractile, ECM-producing myofibroblasts. A key marker of this activation is alpha-smooth muscle actin (αSMA). Among the drivers of this fibrotic response is integrin α11β1, a collagen-binding transmembrane protein encoded by the ITGA11 gene. ITGA11 has been implicated in multiple fibrotic diseases due to its role in enhancing TGFβ1 signaling and promoting myofibroblast activation. To investigate the contribution of ITGA11 to VFS, we performed siRNA-mediated knockdown of ITGA11. We hypothesized that silencing ITGA11 would attenuate myofibroblast activation and reduce fibrotic remodeling in the vocal folds. Our findings support a potential therapeutic role for ITGA11 targeting in the treatment of vocal fold scarring.
Department
Department of Surgery, Division of Otolaryngology, Children’s Hospital of Philadelphia, Philadelphia, PA
Project Mentor
Riccardo Gottardi, PhD
Recommended Citation
Schiffer, Linh P.; Friedman, Ryan M.; Gupta, Yashna; and Gottardi, Riccardo, "Therapeutic Silencing of Integrin α11 Attenuates Myofibroblast Activation in Vocal Fold Fibrosis" (2025). Annual Student Research Poster Session. 227.
https://scholarship.depauw.edu/srfposters/227
Funding and Acknowledgements
The CRISSP Program is supported by the Eunice Kennedy Shriver National Institute of Child Health & Human Development of the National Institutes of Health.