ArticleMolecular biotechnology2022
LncRNA XIST Prevents Tendon Adhesion and Promotes Tendon Repair Through the miR-26a-5p/COX2 Pathway.
Article in Molecular biotechnology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- LncRNA CRNDE regulates the differentiation of tendon-derived stem cells and enhances rotator cuff injury repair by modulating the miR-337/TGFBR2 axis.International journal of clinical and experimental pathology · 2025Article
- Peritendinous adhesion: Therapeutic targets and progress of drug therapy.Computational and structural biotechnology journal · 2024Review
- Unidirectional gene delivery electrospun fibrous membrane via charge repulsion for tendon repair.Bioactive materials · 2024Article
- Advances in non-coding RNA in tendon injuries.Frontiers in genetics · 2024Review
- Advancing Novel Strategies against Post-surgical Tendon Adhesion Bands, Exploring New Frontiers.Current pharmaceutical design · 2024Review
- Reprogramming tendon healing: a guide to novel molecular tools.Frontiers in bioengineering and biotechnology · 2024Review
- Biological and Mechanical Factors and Epigenetic Regulation Involved in Tendon Healing.Stem cells international · 2023Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Tendon adhesion is the biggest obstacle to repair of tendon injury. Long-chain non-coding RNA X-inactive specific transcript (lncRNA XIST) is highly expressed in populations at high risk of tendon injury. However, whether XIST participates in tendon injury and the specific mechanism remain unknown. Here, we aimed to explore the effects and underlying mechanism of XIST in tendon injury. A mouse model of tendon injury was constructed by the transection method in vivo. XIST and COX2 were highly expressed in tendon tissues of mice with tendon injury, while miR-26a-5p was lowly expressed. Fibroblasts were isolated from tendon injury mice. Overexpression of XIST promoted fibroblast proliferation and upregulated α-SMA and Collagen I protein expression, while silencing XIST indicated the opposite effects. Further dual-luciferase reporter gene assay and RIP assay verified a targeting relationship between XIST and miR-26a-5p, as well as miR-26a-5p and COX2, and XIST targeted miR-26a-5p to act on COX2 expression. miR-26a-5p inhibition and COX2 overexpression reversed the decrease in fibroblast proliferation and the downregulation of α-SMA and Collagen I expression caused by XIST silencing, while interference with si-COX2 eliminated the effects of miR-26a-5p inhibitor. This study revealed that XIST promoted fibroblast proliferation and the formation of tendon adhesion through miR-26a-5p/COX2 pathway, suggesting that XIST/miR-26a-5p/COX2 may be a potential target for the treatment of tendon injury.
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Registered trials
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