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Tenascin C Deletion Impairs Tendon Healing and Functional Recovery After Rotator Cuff Repair. | LitMetric

AI Article Synopsis

  • The study investigates how genetic variants of the extracellular matrix protein Tenascin C (TNC) affect healing after rotator cuff repair using a mouse model.
  • Mice lacking TNC exhibited severe tendon and bone defects post-repair and showed reduced physical activity compared to control mice.
  • Results indicated that the absence of TNC altered gene expression related to sex hormones and WNT pathways, suggesting a need for further research to explore tissue-specific changes and potential treatments to improve healing.

Article Abstract

The biological factors that affect healing after rotator cuff repair (RCR) are not well understood. Genetic variants in the extracellular matrix protein Tenascin C () are associated with impaired tendon healing and it is expressed in rotator cuff tendon tissue after injury, suggesting it may have a role in the repair process. The purpose of the current study was to determine the role of TNC on tendon healing after RCR in a murine model. The supraspinatus tendon was transected and repaired on the left shoulder of Wild-Type (WT-RCR), null ( -RCR) and heterozygous ( -RCR) mice. Controls included the unoperated, contralateral shoulder of WT-RCR, RCR, -RCR mice and unoperated shoulders from age and genotype matched controls. We performed histologic, activity testing, RNA-seq, and biomechanical analyses. At 8-weeks post-RCR, and mice had severe bone and tendon defects following rotator cuff repair. -RCR mice had reduced activity after rotator cuff repair including reduced wheel rotations, wheel duration, and wheel episode average velocity compared with WT-RCR. Loss of following RCR altered gene expression in the shoulder, including upregulation of sex hormone and WNT pathways and a downregulation of inflammation and cell cycle pathways. mice had similar biomechanical properties after repair as WT. Further research is required to evaluate tissue specific alterations of , the interactions of and sex hormone and inflammation pathways as well as possible adjuvants to improve enthesis healing in the setting of reduced TNC function.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11419033PMC
http://dx.doi.org/10.1101/2024.09.11.612543DOI Listing

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