Triamcinolone acetonide alters expressions of matrix metalloproteinase-3 gene in primary human chondrocytes
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Creator Monthira Suntiparpluacha, Nattapol Tammachote, Rachaneekorn Tammachote
Title Triamcinolone acetonide alters expressions of matrix metalloproteinase-3 gene in primary human chondrocytes
Publisher Genetics Society of Thailand
Publication Year 2559
Journal Title Genomics and Genetics
Journal Vol. 9
Journal No. 2&3
Page no. 66-71
Keyword chondrocyte, osteoarthritis, glucocorticoid, triamcinolone acetonide, matrix metalloproteinase
ISSN 24655198
Abstract Intra-articular glucocorticoid (GC) injection such as triamcinolone acetonide (TA) is an ultimate pharmaceutical treatment for knee osteoarthritis (OA) patients who do not respond well to other pharmaceutical treatments. Effects of GCs on homeostasis of cartilage extracellular matrix (ECM) are not conclusive. In this study, we investigated whether TA altered expression of genes involved in digestion of collagens and proteoglycans. Chondrocytes isolated from cartilage of ten knee OA patients were treated with TA at 1 and 5 mg/ml. Reverse-transcription real-time polymerase chain reaction (real time RT-PCR) was used to evaluate expressions of genes involving ECM degradation (matrix metalloproteinase (MMP)-1, MMP-3, MMP-13, a disintegrin and metalloproteinase with thrombospondin motives (ADAMTS)-5 and tissue inhibitor of matrix metalloproteinase (TIMP)-3). Analysis of mRNA expression using real time RT-PCR showed that MMP-3 mRNA expressions were significantly increased to 6.59 ? 5.2-fold (p = 0.022) and 5.43 ? 3.46-fold (p < 0.01) in chondrocytes treated with TA at 1 and 5 mg/ml, respectively, as compared to non-treated control. Levels of MMP-1, MMP-13, ADAMTS-5, and TIMP-3 were not significantly changed. Whether TA-increased mRNA expressions of ?MMP-3 in chondrocytes involves degradation of cartilage and accelerates OA progression need further investigations in order to provide information for physicians in TA treatment planning for OA patients.
Genomics and Genetics

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