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| 標題: | Effects of Visfatin on Intracellular Mechanics and Catabolism in Human Primary Chondrocytes through Glycogen Synthase Kinase 3 beta Inactivation |
| 作者: | Chang, Shun-Fu
Huang, Kuo-Chin
Lee, Kuan-Han
Chiang, Yao-Chang
Lee, Wei-Ru
Hsieh, Rong-Ze
Su, Yu-Ping
Wu, Shun-Chi |
| 貢獻者: | Chiayi Chang Gung Mem Hosp, Dept Med Res & Dev
Chiayi Chang Gung Mem Hosp, Dept Orthopaed
Chang Gung Univ, Coll Med
Chia Nan Univ Pharm & Sci, Dept Pharm
Chang Gung Univ Sci & Technol, Chron Dis & Hlth Promot Res Ctr, Dept Nursing, Div Basic Med Sci
Natl Tsing Hua Univ, Dept Engn & Syst Sci
Chang Gung Univ, Coll Med, Grad Inst Clin Med Sci
Vet Gen Hosp, Dept Orthopaed & Traumatol
Natl Yang Ming Univ, Sch Med, Dept Surg |
| 關鍵字: | elasticity
glycogen synthase kinase 3 beta
intracellular mechanics
osteoarthritis
primary human chondrocytes
viscosity
visfatin |
| 日期: | 2021 |
| 上傳時間: | 2023-11-11 11:48:26 (UTC+8) |
| 出版者: | MDPI |
| 摘要: | Osteoarthritis (OA) is still a recalcitrant musculoskeletal disease on account of its complex biochemistry and mechanical stimulations. Apart from stimulation by external mechanical forces, the regulation of intracellular mechanics in chondrocytes has also been linked to OA development. Recently, visfatin has received significant attention because of the clinical finding of the positive correlation between its serum/synovial level and OA progression. However, the precise mechanism involved is still unclear. This study determined the effect of visfatin on intracellular mechanics and catabolism in human primary chondrocytes isolated from patients. The intracellular stiffness of chondrocytes was analyzed by the particle-tracking microrheology method. It was shown that visfatin damages the microtubule and microfilament networks to influence intracellular mechanics to decrease the intracellular elasticity and viscosity via glycogen synthase kinase 3 beta (GSK3 beta) inactivation induced by p38 signaling. Further, microtubule network destruction in human primary chondrocytes is predominantly responsible for the catabolic effect of visfatin on the cyclooxygenase 2 upregulation. The present study shows a more comprehensive interpretation of OA development induced by visfatin through biochemical and biophysical perspectives. Finally, the role of GSK3 beta inactivation, and subsequent regulation of intracellular mechanics, might be considered as theranostic targets for future drug development for OA. |
| 關聯: | INT J MOL SCI, v.22, n.15, pp.8107 |
| 顯示於類別: | [藥學系(所)] 期刊論文
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