Tendon formation and repair rely on specific combinations of transcription factors, growth factors, and mechanical parameters that regulate the production and spatial organization of type I collagen. Here, we investigated the function of the zinc finger transcription factor EGR1 in tendon formation, healing, and repair using rodent animal models and mesenchymal stem cells (MSCs). Adult tendons of Egr1 -/-mice displayed a deficiency in the expression of tendon genes, including Scx, Col1a1, and Col1a2, and were mechanically weaker compared with their WT littermates. EGR1 was recruited to the Col1a1 and Col2a1 promoters in postnatal mouse tendons in vivo. Egr1 was required for the normal gene response following tendon injury in a mouse model of Achilles tendon healing. Forced Egr1 expression programmed MSCs toward the tendon lineage and promoted the formation of in vitro-engineered tendons from MSCs. The application of EGR1-producing MSCs increased the formation of tendon-like tissues in a rat model of Achilles tendon injury. We provide evidence that the ability of EGR1 to promote tendon differentiation is partially mediated by TGF-β2. This study demonstrates EGR1 involvement in adult tendon formation, healing, and repair and identifies Egr1 as a putative target in tendon repair strategies.
We present experimental evidence of self-healing shear cracks at a gel/glass interface. This system exhibits two dynamical regimes depending on the driving velocity: steady sliding at high velocity (>V(c) approximately 100--125 microm/s), characterized by a shear-thinning rheology, and periodic stick-slip dynamics at low velocity. In this last regime, slip occurs by propagation of pulses that restick via a "healing instability" occurring when the local sliding velocity reaches the macroscopic transition velocity V(c). At driving velocities close below V(c), the system exhibits complex spatiotemporal behavior.
Abstract. We present an extensive experimental study and scaling analysis of friction of gelatin gels on glass. At low driving velocities, sliding occurs via propagation of periodic self-healing slip pulses whose velocity is limited by collective diffusion of the gel network. Healing can be attributed to a frictional instability occurring at the slip velocity v = Vc. For v > Vc, sliding is homogeneous and friction is ruled by the shear-thinning rheology of an interfacial layer of thickness of order the (nanometric) mesh size, containing a semi-dilute solution of polymer chain ends hanging from the network. Inspite of its high degree of confinement, the rheology of this system does not differ qualitatively from known bulk ones. The observed ageing of the static friction threshold reveals the slow increase of adhesive bonding between chain ends and glass. Such structural ageing is compatible with the existence of a velocity-weakening regime at velocities smaller than Vc, hence with the existence of the healing instability. PACS
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