Millimeter wave treatment inhibits NO-induced apoptosis of chondrocytes through the p38MAPK pathway

Li, Xihai; Du, Min; Liu, Xianxiang; Wu, Mingxia; Ye, Hongzhi; Lin, Jiumao; Chen, Wenlie; Wu, Guangwen

doi:10.3892/ijmm_00000357

Cited by 21 publications

(27 citation statements)

References 17 publications

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“…As a physical therapeutic regimen, millimeter wave treatment differs from conventional medical regimens in its convenience, safety and non-invasiveness. Our pilot study previously demonstrated that millimeter wave treatment down-regulated the expression and activation of P-p38 and p53 in apoptotic chondrocytes and suppressed the activity of caspase-3, a key player in chondrocytic apoptosis, thus leading to the inhibition of chondrocytic apoptosis (14). As a rapidly responding nuclear transcription factor, a large amount of NF-κB is involved in cell proliferation and immune response.…”

Section: Introductionmentioning

confidence: 99%

In vitro study of inhibitory millimeter wave treatment effects on the TNF-α-induced NF-κB signal transduction pathway

Wu²,

Wu³

et al. 2010

Int J Mol Med

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Abstract. Abnormal activation of the nuclear factor-κB (NF-κB) in chondrocytes initiates the transcription of inflammatory mediators, promotes their generation and release, and amplifies initial inflammatory signals. This results in the release of chondral matrix-degrading enzymes and accelerates the degeneration of articular cartilage. As a non-pharmaceutical and non-invasive physical therapy regimen, millimeter wave treatment has been successfully used for the treatment of osteoarthritis. In this study, chondrocytes were derived from the cartilages of knee joints of 4-week-old male Sprague-Dawley rats and were mechanically digested by collagenase type II treatment for further culture in vitro. The third-passage chondrocytes were stained with toluidine blue and treated with a gradient of tumor necrosis factor-· (TNF-·) for various times. Chondrocytic activity was measured by MTT assay, and the apoptotic rate of the chondrocytes was determined with Hocehst 33342 staining to identify effective treatment concentrations and durations and to establish an apoptosis model for the chondrocytes in response to TNF-·. Using this model, the chondrocytes were randomly divided to receive millimeter wave treatment for various times. The apoptotic rate of the chondrocytes was measured by Annexin V-FITC staining and the protein expression levels of RIP, TAK1, IκB kinase (IKK)-ß, IκB-· and NF-κB, were determined by Western blotting. Chondrocytic structure was examined by transmission electronic microscopy. The apoptotic rates were significantly lower at 4 and 8 h of treatment than at 0 and 2 h. The expression levels of RIP, TAK1, IKK-ß and NF-κB were also significantly lower at 4 and 8 h than at 0 and 2 h, whereas that of IκB-· was significantly higher at 4 and 8 h than at 0 and 2 h. Therefore, we can conclude that millimeter wave treatment can inhibit the activation of the TNF-·-mediated NF-κB signal transduction pathway through the down-regulation of RIP, TAK1, IKK-ß and NF-κB, and the up-regulation of IκB-·, in chondrocytes.

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Section: Introductionmentioning

confidence: 99%

In vitro study of inhibitory millimeter wave treatment effects on the TNF-α-induced NF-κB signal transduction pathway

Wu²,

Wu³

et al. 2010

Int J Mol Med

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“…Millimeter wave is a high-frequency electromagnetic wave at a wavelength from 1-10 mm and a frequency of 300 million cycles/sec (300 MHz) to 300 billion cycles/second (300 GHz) (10,11). The millimeter waves within living organisms generate 0.5x10 10 -3x10 12 coherent oscillations during metabolism, which can be absorbed by biological tissues through resonance to produce a non-thermal biological effect (12).…”

Section: Introductionmentioning

confidence: 99%

Millimeter wave treatment promotes chondrocyte proliferation via G1/S cell cycle transition

et al. 2012

Int J Mol Med

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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 G 1 /S cell cycle progression in chondrocytes and the underlying mecha nism 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 G 0 /G 1 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. IntroductionOsteoarthritis (OA), the most frequent arthropathy, is characterized by progressive degradation of hyaline articular cartilage and is associated with aging (1). A complex interplay of mechanical, and functional changes of chondrocytes could precipitate the imbalance between matrix anabolic and catabolic processes in articular cartilage and thus the pathogenesis of OA (2,3). Chondroctyes can rapidly respond to changes in the articular microenvironment and regulate the dynamic equilibrium between the anabolism and catabolism of the extracellular matrix (ECM), which plays a crucial role in the maintenance of the cartilage function (4). Therefore, enhancing chondrocyte function might be an efficient treatment to cure or even delay the progression of OA by promoting chondrocyte proliferation.The cell cycle plays an important role in the influence on chondrocyte function, which takes place in chondrocytes leading to its division and duplication. Cell cycle control is a highly regulated process that involves a complex cascade of events, in which regulation can be realized through a complicated network by cyclins, cyclin-dependent kinases (CDKs) and cyclin dependent kinase inhibitors (CDKI). G 1 /S transition, one of the two main checkpoints, is a rate-limiting step in the cell cycle and regulates cell proliferation (5,6). Cyclin D1 is a key cell cycle regulatory protein, which binds to CDK4 or CDK6 to control cell cycle progression from the G 1 to the S phase (7). Meanwhile, p21 competes with cyclin D1 for bindin...

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“…This cell type is responsible for repairing damaged cartilage tissue. We previously demonstrated that chondrocytes are obtained by mechanical and chemical isolation methods and that the purity of the isolated chondrocytes is high (14,21). This process provides allowed for the investigation of the effect of MW on chondrocyte apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…MW has been shown to evoke multiple biological effects and is beneficial in the treatment of OA. Recently, we reported that MW inhibited sodium nitroprussiate (SNP)-induced apoptosis of chondrocytes (14). To further explore MW as a potential therapeutic agent in OA, the effect of MW on the mitochondrion-dependent apoptotic pathway in chondrocytes was investigated.…”

Section: Introductionmentioning

confidence: 99%

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Millimeter wave treatment inhibits the mitochondrion-dependent apoptosis pathway in chondrocytes

Sferra

Chen

et al. 2011

Mol Med Report

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Abstract. Millimeter wave (MW) is an electromagnetic wave with a wavelength between 1 and 10 mm and a frequency of 30-300 GHz that causes multiple biological effects, both locally and globally. MW has been widely used in clinical medicine. Although our previous work demonstrated that MW is capable of inhibiting sodium nitroprussiate (SNP)-induced apoptosis in chondrocytes, the precise mechanism of the antiapoptotic activity remains to be elucidated. The purpose of this study was to investigate the effects of MW in SNP-induced apoptotic chondrocytes. Sprague Dawley rat chondrocytes were isolated and cultured, and the cells were counted. Cell viability was evaluated using MTT assay. Cells were then treated with SNP and MW, and flow cytometry was used to detect apoptosis. Our results showed that MW treatment inhibited a SNP-induced mitochondrion-dependent pathway of apoptosis. MW treatment inhibited the loss of plasma membrane asymmetry (externalization of phosphatidylserine), collapse of mitochondrial membrane potential, and activation of caspase-9 and caspase-3. Taken together, the results indicate that MW inhibits the mitochondrion-dependent pathway of apoptosis in chondrocytes and this may, in part, explain its clinical effect in the treatment of osteoarthritis.

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Millimeter wave treatment inhibits NO-induced apoptosis of chondrocytes through the p38MAPK pathway

Cited by 21 publications

References 17 publications

In vitro study of inhibitory millimeter wave treatment effects on the TNF-α-induced NF-κB signal transduction pathway

In vitro study of inhibitory millimeter wave treatment effects on the TNF-α-induced NF-κB signal transduction pathway

Millimeter wave treatment promotes chondrocyte proliferation via G1/S cell cycle transition

Millimeter wave treatment inhibits the mitochondrion-dependent apoptosis pathway in chondrocytes

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