Increasing UCP2 expression and decreasing NOX1/4 expression maintain chondrocyte phenotype by reducing reactive oxygen species production
| Autor: | Jufang Yao, Ping Huang, He Li, Xiang Zhao, Yansong Miao, Yuefu Dong, Zhenyu Huang, Qingrong Xu |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
UCP2
0301 basic medicine chemistry.chemical_classification Reactive oxygen species PGC-1α TFAM Peroxisome Chondrocyte phenotype Cell biology 03 medical and health sciences 030104 developmental biology 0302 clinical medicine chondrocyte phenotype Oncology chemistry Mitochondrial biogenesis NOX1 cardiovascular system NOX1/4 Receptor 030217 neurology & neurosurgery Function (biology) Research Paper |
| Zdroj: | Oncotarget |
| ISSN: | 1949-2553 |
| DOI: | 10.18632/oncotarget.18908 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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