The tenocyte phenotype of human primary tendon cells in vitro is reduced by glucocorticoids

BMC Musculoskeletal Disorders

Research Article

Ludvig J. Backman¹  Jialin Chen¹  Christoph Spang² 

[1] Department of Integrative Medical Biology, Anatomy, Umeå University, SE-901 87, Umeå, Sweden;Department of Integrative Medical Biology, Anatomy, Umeå University, SE-901 87, Umeå, Sweden;Dr Alfen Orthopedic Spine Center, 97080, Würzburg, Germany;

关键词: Dexamethasone;    Scleraxis;    Collagen;    Cell viability;    Phenotype;    Tendinopathy;    Tenocytes;    Tendon cells;   

DOI  :  10.1186/s12891-016-1328-9

 received in 2016-09-05, accepted in 2016-11-04,  发布年份 2016

来源: Springer

【 摘 要 】

BackgroundThe 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.MethodsWe 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 (Alpl, Ocn), cartilage (Acan, Sox9) and fat (Cebpα, Pparg) 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 Col1, Col3 and Col14 was analyzed using qPCR.ResultsStimulation 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 Acan, Alpl and Sox9 were reduced.ConclusionsThese 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.

【 授权许可】

CC BY   
© The Author(s). 2016