title: Diclofenac and triamcinolone acetonide impair tenocytic differentiation and promote adipocytic differentiation of mesenchymal stem cells.
abstract: BACKGROUND
  Tendinopathies are often empirically treated with oral/topical nonsteroidal anti-inflammatory medications and corticosteroid injections despite their unclear effects on tendon regeneration. Recent studies indicate that tendon progenitors exhibit stem cell-like properties, i.e., differentiation to osteoblasts, adipocytes, and chondrocytes, in addition to tenocytes. Our present study aims at understanding the effects of triamcinolone acetonide and diclofenac on tenocytic differentiation of mesenchymal stem cells.
  
  
  METHODS
  The murine fibroblast C3H10T1/2 cell line was induced to tenocytic differentiation by growth differentiation factor-7. Cell proliferation and differentiation with the exposure of different concentrations of triamcinolone acetonide and diclofenac were measured by WST-1 assay and real-time polymerase chain reaction analysis, respectively.
  
  
  RESULTS
  Cell proliferation was decreased in a concentration-dependent manner when exposed to triamcinolone acetonide and diclofenac. In addition to tenocytic differentiation, adipocyte formation was observed, both at gene expression and microscopic level, when the cells were exposed to triamcinolone acetonide or high concentrations of diclofenac.
  
  
  CONCLUSIONS
  Our results indicate that triamcinolone acetonide and diclofenac might alter mesenchymal stem cell differentiation in a nonfavorable way regarding tendon regeneration; therefore, these medications should be used with more caution clinically.
authors.affiliation: Department of Clinical Intervention, Technology and Science, Karolinska Institutet, Stockholm 141 86, Sweden. Maritha.Fredrission@ki.se.
authors.forename: Maritha
authors.initials: M
authors.lastname: Fredriksson
authors.forename: Yan
authors.initials: Y
authors.lastname: Li
authors.forename: Anders
authors.initials: A
authors.lastname: Stålman
authors.forename: Lars-Arne
authors.initials: LA
authors.lastname: Haldosén
authors.forename: Li
authors.initials: L
authors.lastname: Felländer-Tsai
mesh_terms: D017667:Adipocytes / Q000187:drug effects*; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000494:pharmacology; D019485:Bone Morphogenetic Proteins / Q000494:pharmacology; D002454:Cell Differentiation / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D004008:Diclofenac / Q000008:administration & dosage / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D050556:Fatty Acid-Binding Proteins / Q000096:biosynthesis / Q000235:genetics; D005786:Gene Expression Regulation / Q000187:drug effects; D005938:Glucocorticoids / Q000008:administration & dosage / Q000494:pharmacology; D055412:Growth Differentiation Factors / Q000494:pharmacology; D059630:Mesenchymal Stem Cells / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D051379:Mice; D013710:Tendons / Q000166:cytology / Q000187:drug effects*; D014222:Triamcinolone Acetonide / Q000008:administration & dosage / Q000494:pharmacology*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D019485:Bone Morphogenetic Proteins; C493411:Fabp4 protein, mouse; D050556:Fatty Acid-Binding Proteins; C499471:Gdf7 protein, mouse; D005938:Glucocorticoids; D055412:Growth Differentiation Factors; D004008:Diclofenac; D014222:Triamcinolone Acetonide