Abstract
Cross-talk between skeletal muscle and tendon is important for tissue homeostasis. Whereas the skeletal muscle response to tendon injury has been well-studied, to the best of our knowledge the tendon response to skeletal muscle injury has been neglected. Thus, we investigated calcaneal tendon extracellular matrix (ECM) remodeling after gastrocnemius muscle injury using a rat model. Wistar rats were randomly divided into four groups: control group (C; animals that were not exposed to muscle injury) and harvested at different time points post gastrocnemius muscle injury (3, 14, and 28 days) for gene expression, morphological, and biomechanical analyses. At 3 days post injury, we observed mRNA-level dysregulation of signaling pathways associated with collagen I accompanied with disrupted biomechanical properties. At 14 days post injury, we found reduced collagen content histologically accompanied by invasion of blood vessels into the tendon proper and an abundance of peritendinous sheath cells. Finally, at 28 days post injury, there were signs of recovery at the gene expression level including upregulation of transcription factors related to ECM synthesis, remodeling, and repair. At this time point, tendons also presented with increased peritendinous sheath cells, decreased adipose cells, higher Young’s modulus, and lower strain to failure compared to the uninjured controls and all post injury time points. In summary, we demonstrate that the calcaneal tendon undergoes extensive ECM remodeling in response to gastrocnemius muscle injury leading to altered functional properties in a rat model. Tendon plasticity in response to skeletal muscle injury merits further investigation to understand its physiological relevance and potential clinical implications.
Highlights
Acute and chronic tendon disorders, most commonly affecting the calcaneus tendon (CT), account for up to 50% of all sports injuries (Jarvinen et al, 2005b; Egger and Berkowitz, 2017)
In order to evaluate the presence of muscle injury after cryo-lesion, qualitative analysis of histological sections stained with hematoxylin and eosin (HE) was performed in all experimental groups (Figure 1)
This study investigated the effects of skeletal muscle injury on time-course effects on the expression of key genes involved in tendon remodeling as well as the morphological and biomechanical properties of the calcaneal tendon (CT)
Summary
Acute and chronic tendon disorders, most commonly affecting the calcaneus tendon (CT), account for up to 50% of all sports injuries (Jarvinen et al, 2005b; Egger and Berkowitz, 2017). Tendons improve the Tendon Plasticity Following Muscle Injury economy of movement and amplify power output by their spring-like properties (Benjamin et al, 2008; Roberts and Azizi, 2010; Wilson and Lichtwark, 2011; Wang et al, 2012). Tendons perform as mechanical buffers to protect skeletal muscle during contraction (Konow et al, 2012). To perform this range of actions, tendons present abundant specialized extracellular matrix (ECM) resistant to tensile and compressive forces composed of approximately 70% of water by mass and collagen (mostly type I and III), proteoglycans, and other non-collagenous proteins organized in a hierarchical manner (Kjaer, 2004; Lavagnino et al, 2015). The tenocytes transduce muscledependent loads to elicit functional remodeling of the ECM; tendons demonstrate plasticity for dynamic adaptation in response to mechanical demands (Benjamin et al, 2008; Andarawis-Puri et al, 2015; Bohm et al, 2015; Lavagnino et al, 2015)
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