Functional and molecular impact of triamcinolone acetonide on primary human bone marrow mesenchymal stem cells

Joint pain, either traumatic or degenerative, is a common cause of morbidity. Triamcinolone acetonide (TA), a common glucocorticoid, has been used as symptomatic treatment for joint pain for decades. However, besides its relatively short-lived therapeutic effects, TA may have potentially devastating effects by altering the normal healing process to restore and maintain the cellular entities that contribute to tissue regeneration of the synovial joint. Mesenchymal stem cells (MSCs) have been shown to hold great potential in tissue regeneration due to their multipotency in regenerating osteoblasts, chondrocytes and adipocytes and their immunomodulatory properties. So far, it remains largely unclear how TA treatment affects MSC activities. Overall design: Bone Marrow mesenchymal stem cells (MSCs) were plated and subjected to either triamcinolone acetonide 10nM in complete DMEM or in complete DMEM only as control for 24 h. The cells were then collected and lysed in RLT buffer (Qiagen, Germantown, MD, USA) and kept at -80°C