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Updated: Oct 26, 2025
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Applying a Three-dimensional Uniaxial Mechanical Stimulation Bioreactor System to Induce Tenogenic Differentiation of Tendon-Derived Stem Cells
Published on: August 1, 2020
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Mechanical Overloading Induced-Activation of mTOR Signaling in Tendon Stem/Progenitor Cells Contributes to
Daibang Nie1,2, Yiqin Zhou2,3, Wang Wang1
1Department of Immunology, College of Basic Medicine, Chongqing Medical University, Chongqing, China.
Frontiers in Cell and Developmental Biology
|July 29, 2021
Summary
Mechanical loading activates mammalian target of rapamycin (mTOR) in tendon stem cells. Rapamycin treatment prevented tendon degeneration by inhibiting mTOR-driven non-tenocyte differentiation, suggesting a therapeutic approach for tendinopathy.
Area of Science:
- Biomedical Engineering
- Cell Biology
- Orthopedics
Background:
- Tendon homeostasis and pathophysiology are influenced by mechanical loading.
- Molecular mechanisms of mechanotransduction in tendon cells are not fully understood.
Purpose of the Study:
- To investigate the role of mammalian target of rapamycin (mTOR) signaling in tendon stem/progenitor cell (TSC) mechanotransduction.
- To evaluate the potential of mTOR inhibition for preventing tendinopathy.
Main Methods:
- In vitro mechanical loading of rat patellar TSCs.
- Pharmacological inhibition of mTOR using rapamycin.
- Assessment of cell proliferation and differentiation markers.
- In vivo studies using mice subjected to intensive treadmill running (ITR) with rapamycin treatment.
Main Results:
- Mechanical loading activated mTOR in TSCs in a magnitude-dependent manner.
- Rapamycin inhibited mTOR activation, TSC proliferation, and non-tenocyte differentiation.
- ITR induced tendon degeneration in mice, which was ameliorated by rapamycin treatment.
Conclusions:
- Mechanical loading activates mTOR signaling in TSCs.
- Rapamycin can prevent tendinopathy by blocking mTOR-mediated non-tenocyte differentiation in response to mechanical stress.
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