Abstract
The molecular mechanisms of TNF-α-induced apoptosis of chondrocyte and the role of Ca2+ mediating the effects of MW on TNF-α-induced apoptosis of chondrocytes remained unclear. In this study, we investigated the molecular mechanism underlying inhibiting TNF-α-induced chondrocytes apoptosis of MW. MTT assay, DAPI, and flow cytometry demonstrated that MW significantly increased cell activity and inhibited chromatin condensation accompanying the loss of plasma membrane asymmetry and the collapse of mitochondrial membrane potential. Our results also indicated that MW reduced the elevation of [Ca2+]i in chondrocytes by LSCM. Moreover, MW suppressed the protein levels of calpain, Bax, cytochrome c, and caspase-3, while the expressions of Bcl-2, collagen II, and aggrecan were increased. Our evidences indicated that MW treatment inhibited the apoptosis of chondrocytes through depression of [Ca2+]i. It also inhibited calpain activation, which mediated Bax cleavage and cytochrome c release and initiated the apoptotic execution phase. In addition, MW treatment increased the expression of collagen II and aggrecan of chondrocytes.
Highlights
Osteoarthritis (OA) is characterized by a progressive loss of joint articular cartilage caused by the interaction of mechanical and biological factors
Osteoarthritis (OA) is a multifactorial disease characterized by the breakdown of hyaline articular cartilage and the formation of osteophytes
The chondrocyte is the only cell type present in mature cartilage that is responsible for extracellular signals and the maintenance of cartilage homeostasis
Summary
Osteoarthritis (OA) is characterized by a progressive loss of joint articular cartilage caused by the interaction of mechanical and biological factors. The abrasion of articular cartilages stimulates an inflammatory reaction in synovial cells and chondrocytes. The local increase in inflammatory stimuli in the articular tissues leads to secondary synovial proliferation, articular exudation, and cartilage dystrophy, resulting in articular cartilage degeneration [1,2,3,4]. One of the pivotal inflammatory factors, tumor necrosis factor-α (TNF-α), induces inflammation, promotes the release of bone matrix-degrading enzymes, and mediates fibroblastic hyperplasia and histological damage [5, 6]. Depending on the cell type and the state of cellular activation, TNF-α can induce a wide range of biological effects, including cell differentiation, proliferation, apoptosis, and multiple proinflammatory effects [7]. Living organisms generate 0.5 × 1010∼3 × 1012 coherent oscillations during metabolism, which is within the frequency of a millimeter wave. The energy of the MW can be absorbed by biological tissues through resonance, and the energy may interfere with signal transduction and affect metabolism [8,9,10,11,12]
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