Electroacupuncture promotes chondrocyte proliferation via accelerated G1/S transition in the cell cycle

Huang,Yali; Wu,Guangwen; Fan,Huailing; Ye,Jinxia; Liu,Xianxiang

doi:10.3892/ijmm.2013.1336

Electroacupuncture promotes chondrocyte proliferation via accelerated G1/S transition in the cell cycle

Authors:
- Yali Huang
- Guangwen Wu
- Huailing Fan
- Jinxia Ye
- Xianxiang Liu
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Affiliations: College of Orthopedics and Traumatology, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, P.R. China, Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, P.R. China, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, P.R. China, Fujian Key Laboratory of Integrative Medicine on Geriatrics, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, P.R. China
Published online on: April 5, 2013 https://doi.org/10.3892/ijmm.2013.1336
Pages: 1443-1448

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Abstract

The aim of the present study was to investigate the effects of electroacupuncture (EA) on the proliferation of chondrocytes and the molecular mechanism(s) involved. Passage 2 chondrocytes were randomly divided into four groups and treated with EA or nocodazole. After treatment, cell proliferation was determined using an MTT assay and DNA staining followed by FACS. The mRNA expression levels of cyclin D1, cyclin-dependent kinase (CDK)4, CDK6, phosphorylated retinoblastoma (pRb) and P16 were detected by RT-PCR, and the protein levels of cyclin D1, CDK4, CDK6, pRb and P16 were detected by western blotting. EA treatment significantly increased cell viability in a time-dependent manner and decreased the number of G0/G1 and G2/M phase chondrocytes and increased the number of S phase cells. The mRNA and protein levels of cyclin D1, CDK4, CDK6, (p)Rb and P16 consistently demonstrated a reverse trend with the levels in the chondrocytes treated with nocodazole. The expression levels of cyclin D1, CDK4, CDK6 and Rb were higher in chondrocytes receiving EA treatment when compared to levels in the untreated cells while expression of P16 was lower. In conclusion, EA treatment promotes chondrocyte proliferation via promotion of G1/S checkpoint transition in the cell cycle dependent on the activity of the P16-cyclin D1-CDK4/6-pRb pathway and this may, in part, explain its clinical effect in the treatment of osteoarthritis.

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