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頁籤選單縮合
題名 | Mechanotransduction in Normal and Osteoarthritic Human Articular Chondrocytes=人類正常關節與骨關節炎軟骨細胞之機械力訊息傳導 |
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作 者 | 李恆昇; | 書刊名 | Journal of Medical Sciences |
卷期 | 23:4 2003.08[民92.08] |
頁次 | 頁183-189 |
分類號 | 416.61 |
關鍵詞 | 關節; 骨關節炎; 軟骨細胞; Cartilage; Integrin; Mechanotransduction; Osteoarthritis; |
語文 | 英文(English) |
英文摘要 | Articular cartilage requires to be exposed to mechanical stimuli within a physiological range for normal structure and function to be maintained. Mechanotransduction is the process by which mechanical forces are recognized by cells and transduced into a series of intracellular signaling events that in turn regulate cell function. These processes and events are beginning to be defined in healthy diseased cartilage with results of studies indicating the presence of novel signaling pathways that appear to be modified in diseases such as osteoarthritis. Following mechanical simulation of normal articular chondrocytes in vitro there is an elevation in levels of aggrecan mRNA and a decrease in relative levels of MMP3 mRNA. This anabolic response, associated with membrane hyperpolarisation, is dependent upon an integrin-dependent interleukin (IL)-4 autocrine/paracrine loop and involves activation of PKC. Recent studies show involvement of tachykinin signaling. In osteoarthritis this chondroprotective response appears to be lost. The reasons for these major differences remain to be fully established. α5β1 integrin is the mechanoreceptor in chondrocytes from both normal and osteoarthritic (OA) cartilage but downstream signaling pathways appear to differ. OA chondrocytes show membrane depolarisation following 0.33 Hz mechanical stimulation consequent to activation of an IL1βautocrine/paracrine loop. Altered mechanottransduction and signaling in OA may contribute to changes in chondrocyte behavioour leading to increased cartilage breakdown and disease progression. |
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