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Updated: Sep 12, 2025
Murine Flexor Tendon Injury and Repair Surgery
Published on: September 19, 2016
Paclitaxel-mediated microtubule stabilization regulates flexor tendon repair in rats
Juan Juan Yang1, Si Wei Xu1, Xu You Zhang1
1Hand Surgery Research Center & Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, China.
Aims:
Tendon healing is a considerable challenge in hand surgery, and the outcome depends on the function of tenocytes and homeostasis of the extracellular matrix. Although microtubule dynamics play crucial roles in various cellular processes, their function in tenocytes remains unknown. This study aimed to investigate the effects of microtubule-targeting agents (paclitaxel and vincristine) on tenocytes, focusing on their influence on tenocyte proliferation and extracellular matrix synthesis. The regulatory effects of microtubule polymerization on tendon healing were also evaluated in vivo.
Methods:
A total of 200 four-week-old female C57BL/6 mice were euthanized. Tenocytes were isolated from the flexor digitorum profundus tendons of the index, middle, and ring fingers of the hind paws. The tendon cells were exposed to various concentrations (0, 10, 25, 50, 100, and 200 nM) of paclitaxel or vincristine for 24, 48, 72, and 96 hours, respectively. A rat tendon injury model was established by transecting and repairing the flexor digitorum longus (FDL) tendon, and a paclitaxel-loaded GleMA hydrogel delivery system was applied locally.
Results:
We found that both paclitaxel-induced microtubule polymerization and vincristine-induced depolymerization increased the viability of tenocytes. However, only paclitaxel treatment facilitated cell proliferation and stimulated the reorganization of microtubules. Additionally, the expression of cyclin-dependent kinase 1 (CDK1), type III collagen (Col III), and matrix metalloproteinase-3 (MMP-3) was significantly higher when the cells were treated with paclitaxel rather than vincristine treatment. In vivo analysis study using a hydrogel-paclitaxel delivery system revealed significantly improved digit flexion function, increased expression of Col III and MMP-3, and enhanced tissue repair in a rat FDL tendon injury model.
Conclusion:
Paclitaxel-mediated microtubule polymerization promotes tenocyte proliferation and extracellular matrix synthesis, ultimately improving tendon healing in a rat model of flexor tendon injury. These improvements were associated with elevated expression of Col III and MMP-3 in tenocytes.
Insights
Paclitaxel promotes tendon healing by enhancing tenocyte proliferation and extracellular matrix synthesis via microtubule polymerization. This study highlights paclitaxel
Area of Science:
- Cell Biology
- Biomaterials Science
- Orthopedic Surgery
Background:
- Tendon healing is complex, relying on tenocyte function and extracellular matrix (ECM) homeostasis.
- The role of microtubule dynamics in tenocyte function and tendon healing remains largely unexplored.
- Microtubule-targeting agents offer potential tools to modulate cellular processes relevant to tendon repair.
Purpose of the Study:
- To investigate the effects of microtubule-targeting agents (paclitaxel and vincristine) on tenocyte proliferation and ECM synthesis.
- To evaluate the in vivo impact of microtubule polymerization on tendon healing.
Main Methods:
- Tenocytes were isolated and treated with paclitaxel or vincristine at various concentrations and time points.
- Cell proliferation, microtubule reorganization, and expression of key genes (CDK1, Col III, MMP-3) were assessed.
- A rat flexor digitorum longus (FDL) tendon injury model was utilized with a paclitaxel-loaded hydrogel delivery system for in vivo evaluation.
Main Results:
- Both paclitaxel (polymerization) and vincristine (depolymerization) enhanced tenocyte viability.
- Paclitaxel significantly promoted tenocyte proliferation, microtubule reorganization, and increased expression of Col III and MMP-3.
- In vivo, paclitaxel treatment via hydrogel delivery improved digit flexion, enhanced Col III and MMP-3 expression, and accelerated tissue repair.
Conclusions:
- Paclitaxel-mediated microtubule polymerization positively influences tenocyte proliferation and ECM synthesis.
- This mechanism contributes to improved tendon healing in a preclinical model of flexor tendon injury.
- Elevated Col III and MMP-3 expression are key indicators associated with paclitaxel-enhanced tendon repair.
