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- Title
Oxysterol 25-hydroxycholesterol as a metabolic pathophysiological factors of osteoarthritis induces apoptosis in primary rat chondrocytes.
- Authors
Yo-Seob Seo; In-A Cho; Tae-Hyeon Kim; Jae-Seek You; Ji-Su Oh; Gyeong-Je Lee; Do Kyung Kim; Jae-Sung Kim
- Abstract
The aim of the present study was to investigate the pathophysiological etiology of osteoarthritis that is mediated by the apoptosis of chondrocytes exposed to 25-hydroxycholesterol (25-HC), an oxysterol synthesized by the expression of cholesterol-25-hydroxylase (CH25H) under inflammatory conditions. Interleukin-1ß induced the apoptosis of chondrocytes in a dose-dependent manner. Furthermore, the production of 25-HC increased in the chondrocytes treated with interleukin-1ß through the expression of CH25H. 25-HC decreased the viability of chondrocytes. Chondrocytes with condensed nucleus and apoptotic populations increased by 25-HC. Moreover, the activity and expression of caspase-3 were increased by the death ligand-mediated extrinsic and mitochondria-dependent intrinsic apoptotic pathways in the chondrocytes treated with 25-HC. Finally, 25-HC induced not only caspasedependent apoptosis, but also induced proteoglycan loss in articular cartilage ex vivo cultured rat knee joints. These data indicate that 25-HC may act as a metabolic pathophysiological factor in osteoarthritis that is mediated by progressive chondrocyte death in the articular cartilage with inflammatory condition.
- Subjects
CARTILAGE cells; APOPTOSIS inducing factor; ARTICULAR cartilage; KNEE; RATS
- Publication
Korean Journal of Physiology & Pharmacology, 2020, Vol 24, Issue 3, p249
- ISSN
1226-4512
- Publication type
Article
- DOI
10.4196/kjpp.2020.24.3.249