ArticleBMC musculoskeletal disorders2023
Interleukin-6 upregulates extracellular matrix gene expression and transforming growth factor β1 activity of tendon progenitor cells.
Article in BMC musculoskeletal disorders, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Parameter-screened LED therapy targets STAT3/IL-6 axis to attenuate tendinopathy via dual modulation of inflammation and ECM remodeling.Journal of orthopaedic surgery and research · 2026Article
- Comparative analysis of different macromolecular crowding agents in human tenocyte cultures.Biomaterials and biosystems · 2026Article
- Decoding Causal Associations Between Neuropsychiatric Disorders and Rotator Cuff Tendinopathy: A Two-Sample Mendelian Randomization Study.Brain and behavior · 2026Article
- Engineering DNA Origami Captors for TGFβ1 Sequestration to Enhance Tumor Immune Modulation and Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Unravelling the role of interleukin-6 in regulating dental stem cell behaviour: a scoping review.BMC oral health · 2025Article
- Therapeutic Potential of Mesenchymal Stem Cell and Tenocyte Secretomes for Tendon Repair: Proteomic Profiling and Functional Characterization In Vitro and In Ovo.International journal of molecular sciences · 2025Article
- IL-1β + TGF-β2 dual-licensed mesenchymal stem cells have reduced major histocompatibility class I expression and positively modulate tenocyte migration, metabolism, and gene expression.Journal of the American Veterinary Medical Association · 2024Article
- The modulating role of uniaxial straining in the IL-1β and TGF-β mediated inflammatory response of human primary ligamentocytes.Frontiers in bioengineering and biotechnology · 2024Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundProlonged inflammation during tendon healing and poor intrinsic healing capacity of tendon are causal factors associated with tendon structural and functional degeneration. Tendon cells, consisting of mature tenocytes and tendon progenitor cells (TPC) function to maintain tendon structure via extracellular matrix (ECM) synthesis. Tendon cells can succumb to tissue cytokine/chemokine alterations during healing and consequently contribute to tendon degeneration. Interleukin-(IL-)1β, IL-6 and TNFα are key cytokines upregulated in injured tendons; the specific effects of IL-6 on flexor tendon-derived TPC have not been discerned.
methodsPassage 3 equine superficial digital flexor tendon (SDFT)-derived TPC were isolated from 6 horses. IL-6 impact on the viability (MMT assay with 0, 1, 5 and 10 ng/mL concentrations), migration (scratch motility assay at 0, 10ng/mL concentration) of TPC in monolayer culture were assessed. IL-6 effect on tendon ECM and chondrogenic gene expression (qRT-PCR), TGFβ1 gene expression and activity (ELISA), and MMP-1, -3 and - 13 gene expression of TPC was evaluated.
resultsIL-6 decreased TPC viability and migration. IL-6 treatment at 10 ng/mL significantly up-regulated TGFβ1 gene expression (6.3-fold; p = 0.01) in TPC, and significantly increased the TGFβ1 concentration in cell culture supernates. IL-6 (at 10 ng/mL) significantly up-regulated both tendon ECM (COL1A1:5.3-fold, COL3A1:5.4-fold, COMP 5.5-fold) and chondrogenic (COL2A1:3.9-fold, ACAN:6.2-fold, SOX9:4.8-fold) mRNA expression in TPC. Addition of SB431542, a TGFβ1 receptor inhibitor, to TPC in the presence of IL-6, attenuated the up-regulated tendon ECM and chondrogenic genes.
conclusionIL-6 alters TPC phenotype during in vitro monolayer culture. Pro- and anti-inflammatory roles of IL-6 have been implicated on tendon healing. Our findings demonstrate that IL-6 induces TGFβ1 activity in TPC and affects the basal TPC phenotype (as evidenced via increased tendon ECM and chondrogenic gene expressions). Further investigation of this biological link may serve as a foundation for therapeutic strategies that modulate IL-6 to enhance tendon healing.
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