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The tenocyte phenotype of human primary tendon cells in vitro is reduced by glucocorticoids
Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB), Anatomy. Dr Alfen Orthopedic Spine Center, 97080 Würzburg, Germany.
Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB), Anatomy.
Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB), Anatomy.
2016 (English)In: BMC Musculoskeletal Disorders, ISSN 1471-2474, E-ISSN 1471-2474, Vol. 17, 467Article in journal (Refereed) Published
Abstract [en]

Background: The use of corticosteroids (e.g., dexamethasone) as treatment for tendinopathy has recently been questioned as higher risks for ruptures have been observed clinically. In vitro studies have reported that dexamethasone exposed tendon cells, tenocytes, show reduced cell viability and collagen production. Little is known about the effect of dexamethasone on the characteristics of tenocytes. Furthermore, there are uncertainties about the existence of apoptosis and if the reduction of collagen affects all collagen subtypes.

Methods: We evaluated these aspects by exposing primary tendon cells to dexamethasone (Dex) in concentrations ranging from 1 to 1000 nM. Gene expression of the specific tenocyte markers scleraxis (Scx) and tenomodulin (Tnmd) and markers for other mesenchymal lineages, such as bone (AlplOcn), cartilage (AcanSox9) and fat (CebpαPparg) was measured via qPCR. Cell viability and proliferation was calculated using a MTS Assay. Cell death was measured by LDH assay and cleaved caspase-3 using Western Blot. Gene expression of collagen subtypes Col1Col3 and Col14 was analyzed using qPCR.

Results: Stimulation with Dex decreased cell viability and LDH levels. Dex also induced a significant reduction of Scx gene expression and a marked loss of fibroblast like cell shape. The mRNA for all examined collagen subtypes was found to be down-regulated. Among non-tendinous genes only Pparg was significantly increased, whereas AcanAlpl and Sox9 were reduced.

Conclusions: These results indicate a Dex induced phenotype drift of the tenocytes by reducing scleraxis expression. Reduction of several collagen subtypes, but not cell death, seems to be a feature of Dex induced tissue degeneration.

Place, publisher, year, edition, pages
2016. Vol. 17, 467
Keyword [en]
Dexamethasone, Scleraxis, Collagen, Cell viability, Phenotype, Tendinopathy
National Category
Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:umu:diva-133277DOI: 10.1186/s12891-016-1328-9ISI: 000395053500002PubMedID: 27832770OAI: oai:DiVA.org:umu-133277DiVA: diva2:1087277
Available from: 2017-04-06 Created: 2017-04-06 Last updated: 2017-04-06Bibliographically approved

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