Abstract
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.
Highlights
Despite the significant efforts toward improving tendon healing and regeneration, the specific cellular contributions during tendon healing have not been extensively characterized (Nichols et al, 2019)
At 38 days post-depletion, total tendon cells were reduced by 60.42% (p
Previous work has established the importance of Scx expression in tendon development (Murchison et al, 2007), growth (Gumucio et al, 2020), and healing (Sakabe et al, 2018), but few studies have considered the direct contributions of ScxLin tendon cells to these processes
Summary
Despite the significant efforts toward improving tendon healing and regeneration, the specific cellular contributions during tendon healing have not been extensively characterized (Nichols et al, 2019). Scx-GFP mice (Pryce et al, 2007) have been used to visualize tendon cells in many studies; previous work has suggested that extrinsic, paratenon-derived Scx-GFP- cells can turn on Scx expression and become Scx-GFP+ by 14 days in a Patellar tendon injury model (Dyment et al., 2014). We have previously demonstrated that ScxAi9 tendon cells organize into a linear, cellular bridge spanning the scar tissue between the tendon stubs following acute injury and repair of the adult flexor digitorum longus (FDL) tendon (Best and Loiselle, 2019). While these studies suggest that tendon type We examined alterations in wound healingrelated cell populations, transcriptomics via RNA sequencing, and the effects of ScxLin cell depletion on tendon post-natal growth and homeostasis
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