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Cell autonomous TGF-beta signaling is essential for cell recruitment into degenerating tendons

Tan, G.-K.; Pryce, B. A.; Stabio, A.; Keene, D. R.; Tufa, S. F.; Schweitzer, R.

2020-11-11 cell biology
10.1101/2020.11.11.378505 bioRxiv
Show abstract

Understanding the role of cell recruitment in tendon disorders is critical for improvements in regenerative therapy. We recently reported that targeted disruption of TGF{beta} type II receptor in the tendon cell lineage (Tgfbr2ScxCre) resulted in tenocyte dedifferentiation and tendon degradation in post-natal stages. Here we extend the analysis and identify direct recruitment of stem/progenitor cells into the degenerative mutant tendons. Cre-lineage tracing indicates that these cells are not derived from tendon ensheathing tissues or from a Scleraxis-lineage, and they turned on tendon markers only upon entering the mutant tendons. Through immunohistochemistry and inducible gene deletion, we further find that the recruited cells originated from a Sox9-expressing lineage and their recruitment was dependent on cell-autonomous TGF{beta} signaling. These results thus differ from previous reports of cell recruitment into injured tendons, and suggest a critical role for TGF{beta} signaling and cell recruitment in the etiology and treatment of tendon degeneration.

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