title: Millimeter wave treatment promotes chondrocyte proliferation via G1/S             cell cycle transition.
abstract: Millimeter waves, high-frequency electromagnetic waves, can effectively alleviate the clinical symptoms in osteoarthritis patients, as a non-pharmaceutical and non-invasive physical therapy regimen. However, the molecular mechanisms of the therapeutic effects of millimeter wave treatment are not well understood. In the present study, the effect of millimeter waves on the G1/S cell cycle progression in chondrocytes and the underlying mechanism was investigated. Chondrocytes isolated from the knee of SD rats were cultured and identified using toluidine blue staining. The second generation chondrocytes were collected and stimulated with or without millimeter waves for 48 h. Chondrocyte viability was analyzed using the MTT assay. The cell cycle distribution of chondrocytes was analyzed by flow cytometry. mRNA and protein expression levels of cyclin D1, cyclin-dependent kinases 4 and 6 (CDK4 and CDK6) and p21 were detected using real-time PCR and western blotting, respectively. Millimeter wave stimulation was found to significantly enhance chondrocyte viability. Moreover, the percentage of chondrocytes in the G0/G1 phase was significantly decreased, whereas that in the S phase was significantly increased. In addition, following millimeter wave treatment, cyclin D1, CDK4 and CDK6 expression was significantly upregulated, whereas p21 expression was significantly downregulated. The results indicate that millimeter wave treatment promotes chondrocyte proliferation via cell cycle progression.
authors.affiliation: Academy of Integrative Medicine, Fujian University of Traditional                     Chinese Medicine, Fuzhou 350108, P.R. China.
authors.forename: Xihai
authors.initials: X
authors.lastname: Li
authors.forename: Hongzhi
authors.initials: H
authors.lastname: Ye
authors.forename: Fangrong
authors.initials: F
authors.lastname: Yu
authors.forename: Liangliang
authors.initials: L
authors.lastname: Cai
authors.forename: Huiting
authors.initials: H
authors.lastname: Li
authors.forename: Jiashou
authors.initials: J
authors.lastname: Chen
authors.forename: Mingxia
authors.initials: M
authors.lastname: Wu
authors.forename: Wenlie
authors.initials: W
authors.lastname: Chen
authors.forename: Ruhui
authors.initials: R
authors.lastname: Lin
authors.forename: Zuanfang
authors.initials: Z
authors.lastname: Li
authors.forename: Chunsong
authors.initials: C
authors.lastname: Zheng
authors.forename: Huifeng
authors.initials: H
authors.lastname: Xu
authors.forename: Guangwen
authors.initials: G
authors.lastname: Wu
authors.forename: Xianxiang
authors.initials: X
authors.lastname: Liu
mesh_terms: D000818:Animals; D049109:Cell Proliferation; D002470:Cell Survival; D002478:Cells, Cultured; D019902:Chondrocytes / Q000166:cytology* / Q000378:metabolism / Q000648:ultrastructure; D019938:Cyclin D1 / Q000235:genetics; D051358:Cyclin-Dependent Kinase 4 / Q000235:genetics; D051361:Cyclin-Dependent Kinase 6 / Q000235:genetics; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000235:genetics; D004574:Electromagnetic Fields; D016193:G1 Phase; D005786:Gene Expression Regulation; D007719:Knee Joint / Q000166:cytology; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D016196:S Phase
chemical_list: D050759:Cyclin-Dependent Kinase Inhibitor p21; D019938:Cyclin D1; D051358:Cyclin-Dependent Kinase 4; D051361:Cyclin-Dependent Kinase 6