Effects of Visfatin on Intracellular Mechanics and Catabolism in Human Primary Chondrocytes through Glycogen Synthase Kinase 3 beta Inactivation

doi:10.3390/ijms22158107

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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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