Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, United States
Antonion Korcari
Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, United States; Department of Biomedical Engineering, University of Rochester, New York, United States
Keshia E Mora
Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, United States; Department of Biomedical Engineering, University of Rochester, New York, United States
Anne EC Nichols
Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, United States
Samantha N Muscat
Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, United States
Emma Knapp
Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, United States
Mark R Buckley
Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, United States; Department of Biomedical Engineering, University of Rochester, New York, United States
Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, United States; Department of Biomedical Engineering, University of Rochester, New York, United States
Despite the requirement for Scleraxis-lineage (ScxLin) cells during tendon development, the function of ScxLin cells during adult tendon repair, post-natal growth, and adult homeostasis have not been defined. Therefore, we inducibly depleted ScxLin cells (ScxLinDTR) prior to tendon injury and repair surgery and hypothesized that ScxLinDTR mice would exhibit functionally deficient healing compared to wild-type littermates. Surprisingly, depletion of ScxLin cells resulted in increased biomechanical properties without impairments in gliding function at 28 days post-repair, indicative of regeneration. RNA sequencing of day 28 post-repair tendons highlighted differences in matrix-related genes, cell motility, cytoskeletal organization, and metabolism. We also utilized ScxLinDTR mice to define the effects on post-natal tendon growth and adult tendon homeostasis and discovered that adult ScxLin cell depletion resulted in altered tendon collagen fibril diameter, density, and dispersion. Collectively, these findings enhance our fundamental understanding of tendon cell localization, function, and fate during healing, growth, and homeostasis.
