Increasing UCP2 expression and decreasing NOX1/4 expression maintain chondrocyte phenotype by reducing reactive oxygen species production
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Yansong Miao1,*, Yuefu Dong2,*, Ping Huang1, Xiang Zhao1, Zhenyu Huang3, Jufang Yao4, He Li5 and Qingrong Xu1
1Department of Orthopaedics, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China
2Department of Joint Surgery, The First People’s Hospital of Lianyungang, Lianyungang, China
3Department of Cerebral Surgery, Tong Ren Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China
4Department of Animal Facility, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China
5Department of Traditional Chinese Medicine, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China
*These authors have contributed equally to this work
Qingrong Xu, email: [email protected]
He Li, email: [email protected]
Keywords: UCP2, NOX1/4, PGC-1α, TFAM, chondrocyte phenotype
Received: November 15, 2016 Accepted: May 06, 2017 Published: July 01, 2017
The aim of this study is to demonstrate that improving the mitochondrial function can inhibite the loss of chondrocyte phenotype by regulating the expression of uncoupling protein 2(UCP2) and NADPH oxidase1/4(NOX1/4) to reduce the production of reactive oxygen species(ROS). The effects of mitochondrial biogenesis “master regular” peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α), mitochondrial transcriptional factor A (TFAM), UCP2, and NOX1/4 on chondrocyte phenotype was examined. It was found that when the chondrocyte phenotype was lost, PGC-1α, UCP2, and TFAM expression decreased, while NOX1/4 expression increased. Inhibiting UCP2 expression promoted the loss of chondrocyte phenotype, and inhibiting NOX1/4 relieved the loss of the chondrocyte phenotype. After activating the PGC-1α-TFAM pathway, UCP2 increased and NOX1/4 decreased, which suppressed loss of the chondrocyte phenotype. After inhibiting NOX1/4, UCP2 expression increased. Increasing and decreasing UCP2 and NOX1/4 expression, respectively, helps maintain the chondrocyte phenotype and improve mitochondrial functioning by reducing reactive oxygen species production.
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