Oncotarget

Research Papers:

Increasing UCP2 expression and decreasing NOX1/4 expression maintain chondrocyte phenotype by reducing reactive oxygen species production

Yansong Miao, Yuefu Dong, Ping Huang, Xiang Zhao, Zhenyu Huang, Jufang Yao, He Li and Qingrong Xu _

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2017; 8:63750-63763. https://doi.org/10.18632/oncotarget.18908

Metrics: PDF 1823 views  |   HTML 2330 views  |   ?  


Abstract

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

Correspondence to:

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

ABSTRACT

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.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 18908