Literature DB >> 29201214

Sirt1 regulates apoptosis and extracellular matrix degradation in resveratrol-treated osteoarthritis chondrocytes via the Wnt/β-catenin signaling pathways.

Shuan Liu1, Hongping Yang1, Bing Hu1, Mingyong Zhang1.   

Abstract

Osteoarthritis (OA) has become a major public health problem with the increased aging population. Previous studies have demonstrated that resveratrol (RES) was able to increase the level of sirtuin 1 (Sirt1) in OA chondrocytes. However, further investigations are required to elucidate the precise molecular mechanism of RES and the potential link between Sirt1 and RES. Therefore, the present study used 30 clinical OA chondrocyte to examine chondrocyte viability, apoptosis rate and the mRNA and protein expression levels of Sirt1 and relevant genes implicated in apoptosis, extracellular matrix (ECM) degradation and Wnt/β-catenin signaling pathway. RES and nicotinamide were used as the stimulus and inhibitor, respectively. The results demonstrated that the apoptotic rate reduced as the cell population decreased from 13.83 to 6.55% in response to 10 µM RES. Expression levels of B-cell lymphoma 2 (Bcl-2) associated X protein (Bax), procaspase-3 and -9, matrix metalloproteinase 1 (MMP1), MMP3, MMP13, Wnt3a, Wnt5a, Wnt7a and β-catenin were significantly inhibited (P<0.01), whereas the level of Bcl-2 was significantly increased (P<0.01) in OA chondrocytes treated with 10 µM RES. These observations suggested that Sirt1 may regulate apoptosis and ECM degradation in RES-treated osteoarthritis chondrocytes via the Wnt/β-catenin signaling pathway.

Entities:  

Keywords:  Wnt/β-catenin signaling; apoptosis; chondrocyte; matrix metalloproteinase; osteoarthritis; sirtuin 1

Year:  2017        PMID: 29201214      PMCID: PMC5704318          DOI: 10.3892/etm.2017.5165

Source DB:  PubMed          Journal:  Exp Ther Med        ISSN: 1792-0981            Impact factor:   2.447


  33 in total

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  20 in total

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Review 6.  The role of sirtuin 1 and its activator, resveratrol in osteoarthritis.

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