Download Full Text (761 KB)


Optimal cellular mechanotransduction is essential for tendon matrix homeostasis. We recently developed an in vivo rat model of tendinosis, where the plantaris tendon are overloaded through ablation of the synergistic Achilles tendon. Using this model we determined that tissue overload disrupts matrix-cell interactions, which results in under-stimulation of tendon cells (tenocytes) (Fig.1)

Using an ex vivo model of tendon stress deprivation by maintaining tail tendon fascicles in floating culture we showed that tenocyte under-stimulation results in destabilization of filamentous (F-)actin (Fig.2). F-actin destabilization coincides with tendinosis-like gene expression: downregulation of tenogenic genes (Col1, Tnc, asma, Scx), upregulation of chondrogenic (Acan, Sox9) and matrix metalloproteinases (Mmp-3, Mmp-13).²

Figure 2. Whole mount confocal images of tail tendons stained for G- and F-actin (DNAse-I and Phallodin, respectively) The mechanisms regulating gene expression by F-actin depolymerization are unknown in tendon. However, we have shown in other cell types (chondrocytes, lens epithelial cells) that F-actin depolymerization regulates gene expression by a G-actin binding transcription factor, myocardin related transcription factor.³

Publication Date



health, tendinosis, actin depolymerization


Medical Genetics | Medicine and Health Sciences | Musculoskeletal System


Presented at the 2024 AOA Research Symposium.

Actin Depolymerization of Tenocytes Promotes a Tendinosis-like Gene Expression