ArticleBone & joint research2025
Paclitaxel-mediated microtubule stabilization regulates flexor tendon repair in rats.
Article in Bone & joint research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
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.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.